1-anilino-8-naphthalenesulfonate has been researched along with Non-alcoholic Fatty Liver Disease in 378 studies
1-anilino-8-naphthalenesulfonate: RN given refers to parent cpd
8-anilinonaphthalene-1-sulfonic acid : A naphthalenesulfonic acid that is naphthalene-1-sulfonic acid substituted by a phenylamino group at position 8.
Non-alcoholic Fatty Liver Disease: Fatty liver finding without excessive ALCOHOL CONSUMPTION.
| Excerpt | Relevance | Reference |
|---|---|---|
| "We previously demonstrated that children with Down syndrome (DS) exhibited a greater risk of steatosis than the general pediatric population." | 7.96 | PNPLA3 gene polymorphism is associated with liver steatosis in children with Down syndrome. ( Alisi, A; Crudele, A; Di Camillo, C; Mosca, A; Novelli, A; Raponi, M; Sartorelli, MR; Scoppola, V; Tarani, L; Valentini, D; Villani, A, 2020) |
| "The aim of the present genetic association study was to test whether overweight/obese carriers of the PNPLA3 148M mutant allele had lower circulating concentrations of retinol than individuals who are homozygous for the 148I allele." | 7.81 | PNPLA3 I148M Variant Influences Circulating Retinol in Adults with Nonalcoholic Fatty Liver Disease or Obesity. ( Albanes, D; Dongiovanni, P; Mancina, RM; Merlo, A; Mondul, A; Montalcini, T; Rametta, R; Romeo, S; Valenti, L, 2015) |
| "Non‑alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease, and has high rates of morbidity and mortality worldwide." | 5.51 | Effects of daphnetin on lipid metabolism, insulin resistance and oxidative stress in OA‑treated HepG2 cells. ( Chen, Y; Han, F; Liao, L; Liu, Y, 2019) |
| "Non-alcoholic fatty liver disease (NAFLD) is one of the most prevalent liver diseases around the world, and is closely associated with obesity, diabetes, and insulin resistance." | 5.40 | Therapeutic role of ursolic acid on ameliorating hepatic steatosis and improving metabolic disorders in high-fat diet-induced non-alcoholic fatty liver disease rats. ( Guo, F; Li, S; Li, X; Li, Y; Liao, X; Meng, F; Meng, M; Sun, C; Sun, Z; Wang, Y, 2014) |
| "We previously demonstrated that children with Down syndrome (DS) exhibited a greater risk of steatosis than the general pediatric population." | 3.96 | PNPLA3 gene polymorphism is associated with liver steatosis in children with Down syndrome. ( Alisi, A; Crudele, A; Di Camillo, C; Mosca, A; Novelli, A; Raponi, M; Sartorelli, MR; Scoppola, V; Tarani, L; Valentini, D; Villani, A, 2020) |
| "The aim of the present genetic association study was to test whether overweight/obese carriers of the PNPLA3 148M mutant allele had lower circulating concentrations of retinol than individuals who are homozygous for the 148I allele." | 3.81 | PNPLA3 I148M Variant Influences Circulating Retinol in Adults with Nonalcoholic Fatty Liver Disease or Obesity. ( Albanes, D; Dongiovanni, P; Mancina, RM; Merlo, A; Mondul, A; Montalcini, T; Rametta, R; Romeo, S; Valenti, L, 2015) |
| "05) with serum levels of alanine aminotransferase (ALT), asparate aminotransferase (AST), glucose, fibrinogen, and insulin-dependent diabetes mellitus, homeostasis model assessment-insulin resistance, and presence of NASH." | 3.79 | Interactions of allelic variance of PNPLA3 with nongenetic factors in predicting nonalcoholic steatohepatitis and nonhepatic complications of severe obesity. ( Charlton, MR; Gawrieh, S; Guichelaar, MM; Krishnan, A; Malinchoc, M; Olivier, M; Sanderson, S; Sarr, M; Swain, JM; Viker, K; Watt, KD, 2013) |
| "Nonalcoholic fatty liver disease (NAFLD) among Latinos is partially attributed to a prevalent C>G polymorphism in the patatin-like phospholipase 3 (PNPLA3) gene." | 3.11 | Clinical Intervention to Reduce Dietary Sugar Does Not Affect Liver Fat in Latino Youth, Regardless of PNPLA3 Genotype: A Randomized Controlled Trial. ( Alderete, TL; Allayee, H; Berger, PK; Cai, Z; Corona, Y; Fogel, J; Goran, MI; Hampson, H; Harlan, G; Hartiala, JA; Jones, RB; Kohli, R; Mack, WJ; Nayak, KS; Pickering, TA; Plows, JF; Rios, C; Salvy, SJ; Schmidt, KA; Sinatra, FR, 2022) |
| "These mutated genes affect NAFLD by promoting liver steatosis (PNPLA3, MBOAT7, TM2SF6, PTPRD, FNDC5, IL-1B, PPARGC1A, UCP2, TCF7L2, SAMM50, IL-6, AGTR1, and NNMT), inflammation (PNPLA3, TNF-α, AGTR1, IL-17A, IL-1B, PTPRD, and GATAD2A), and fibrosis (IL-1B, PNPLA3, MBOAT7, TCF7L2, GATAD2A, IL-6, NNMT, UCP, AGTR1, and TM2SF6)." | 2.82 | Update on Non-Alcoholic Fatty Liver Disease-Associated Single Nucleotide Polymorphisms and Their Involvement in Liver Steatosis, Inflammation, and Fibrosis: A Narrative Review ( Dwi Astarini, F; Ratnasari, N; Wasityastuti, W, 2022) |
| "Since NAFLD has been reported to be associated with lipid metabolism, this study is conducted to explore whether the rs738409 polymorphism of PNPLA3 was associated with lipid levels." | 2.82 | Associations of PNPLA3 rs738409 Polymorphism with Plasma Lipid Levels: A Systematic Review and Meta-Analysis. ( Fang, Y; Li, H; Lin, X; Liu, Y; Luo, Z; Peng, Y; Wan, J; Wei, B; Zhou, Y, 2022) |
| "One hundred three patients with NAFLD were randomised to omega-3 fatty acids (DHA+EPA) or placebo for 15-18months in a double blind placebo controlled trial." | 2.80 | Treating liver fat and serum triglyceride levels in NAFLD, effects of PNPLA3 and TM6SF2 genotypes: Results from the WELCOME trial. ( Bhatia, L; Burdge, GC; Byrne, CD; Calder, PC; Clough, GF; Hoile, SP; Lillycrop, KA; McCormick, KG; Scorletti, E; West, AL, 2015) |
| "We found significant associations with NAFLD at variants in PNPLA3 and GCKR but not in NCAN, LYPLAL1, and PPP1R3B." | 2.79 | Genetic variants in GCKR and PNPLA3 confer susceptibility to nonalcoholic fatty liver disease in obese individuals. ( Chang, MH; Chang, PF; Lin, YC; Ni, YH, 2014) |
| "We examined the genetic background of nonalcoholic fatty liver disease (NAFLD) in the Japanese population, by performing a genome-wide association study (GWAS)." | 2.78 | Genome-wide scan revealed that polymorphisms in the PNPLA3, SAMM50, and PARVB genes are associated with development and progression of nonalcoholic fatty liver disease in Japan. ( Chayama, K; Hotta, K; Hyogo, H; Kitamoto, A; Kitamoto, T; Mizusawa, S; Nakajima, A; Nakamura, T; Nakao, K; Ochi, H; Sekine, A; Teranishi, H; Ueno, T; Yoneda, M, 2013) |
| "Sixty children with NAFLD were randomized in equal numbers to DHA 250 mg/day, DHA 500 mg/day or placebo." | 2.78 | The I148M variant of PNPLA3 reduces the response to docosahexaenoic acid in children with non-alcoholic fatty liver disease. ( Alisi, A; Bedogni, G; Donati, B; Nobili, V; Valenti, L, 2013) |
| "PNPLA3 rs738409 increased the OR of NAFLD by 1." | 2.78 | A common variant in the peroxisome proliferator-activated receptor-γ coactivator-1α gene is associated with nonalcoholic fatty liver disease in obese children. ( Chang, MH; Chang, PF; Lin, YC; Ni, YH, 2013) |
| "Nonalcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver diseases worldwide, including in Japan." | 2.72 | Clinical practice advice on lifestyle modification in the management of nonalcoholic fatty liver disease in Japan: an expert review. ( Fujii, H; Fukunishi, S; Kamada, Y; Kawaguchi, T; Nakajima, A; Okanoue, T; Seko, Y; Shimizu, M; Sumida, Y; Takahashi, H; Tokushige, K, 2021) |
| "Non-alcoholic fatty liver disease (NAFLD) is one of the most common causes of hepatic disorders." | 2.72 | A review of non-alcoholic fatty liver disease in non-obese and lean individuals. ( Ahadi, M; Farzanehfar, M; Masoudifar, N; Molooghi, K; Namdar, AB; Vossoughinia, H, 2021) |
| "Epidemiological studies indicate that NAFLD raises risk of fatal or non-fatal CVD events." | 2.72 | Nonalcoholic fatty liver disease or metabolic dysfunction-associated fatty liver disease diagnoses and cardiovascular diseases: From epidemiology to drug approaches. ( Corsini, A; Dongiovanni, P; Paolini, E; Ruscica, M; Sirtori, CR, 2021) |
| "Non-alcoholic fatty liver disease (NAFLD) is a common disorder that is known to be the leading cause of chronic liver disease worldwide." | 2.72 | Association between PNPLA3 rs738409 polymorphism and nonalcoholic fatty liver disease: a systematic review and meta-analysis. ( Darvishi, F; Darvishi, N; Ghasemi, H; Hosseinian-Far, M; Mansouri, K; Mohammadi, M; Salari, N, 2021) |
| "Nonalcoholic fatty liver disease (NAFLD) affects around a quarter of the global population, paralleling worldwide increases in obesity and metabolic syndrome." | 2.66 | Genetic contributions to NAFLD: leveraging shared genetics to uncover systems biology. ( Eslam, M; George, J, 2020) |
| "Non-alcoholic fatty liver disease (NAFLD) is highly prevalent among individuals with type 2 diabetes." | 2.66 | Non-alcoholic fatty liver disease and cardiovascular disease: assessing the evidence for causality. ( Brouwers, MCGJ; Isaacs, A; Simons, N; Stehouwer, CDA, 2020) |
| "However, whilst the association between NAFLD and risk of prevalent CKD is strong across various patient populations, whether NAFLD is independently associated with the development and progression of CKD is still debatable." | 2.66 | Risk of Kidney Dysfunction IN Nafld. ( Buzzetti, E; Dalbeni, A; Grani, G; Mantovani, A; Zusi, C, 2020) |
| "Non-alcoholic fatty liver disease (NAFLD) includes liver diseases ranging from simple steatosis to progressive forms characterized by high rates of complications and mortality, namely fibrosis, cirrhosis and hepatocellular carcinoma." | 2.66 | Combined use of Genetic Polymorphisms and Elastographic Techniques in NAFLD: Fact or Fiction? ( Fargion, S; Fracanzani, AL; Lombardi, R, 2020) |
| "Furthermore, it also indicated that nonalcoholic steatohepatitis (NASH) was more frequently observed in G allele carriers among paediatric and adolescent NAFLD patients." | 2.66 | Effect of the patatin-like phospholipase domain containing 3 gene (PNPLA3) I148M polymorphism on the risk and severity of nonalcoholic fatty liver disease and metabolic syndromes: A meta-analysis of paediatric and adolescent individuals. ( Hua, W; Ji, C; Li, J; Rui, J; Shi, B; Xie, C; Yang, X; Zhao, Y, 2020) |
| "Nonalcoholic fatty liver disease (NAFLD) is on the verge of becoming the leading cause of liver disease." | 2.66 | Toward Genetic Prediction of Nonalcoholic Fatty Liver Disease Trajectories: PNPLA3 and Beyond. ( Krawczyk, M; Lammert, F; Liebe, R, 2020) |
| "Nonalcoholic fatty liver disease (NAFLD), including nonalcoholic steatohepatitis (NASH), causes hepatic fibrosis, cirrhosis and hepatocellular carcinoma (HCC)." | 2.66 | Molecular Mechanisms: Connections between Nonalcoholic Fatty Liver Disease, Steatohepatitis and Hepatocellular Carcinoma. ( Goto, T; Hirotsu, Y; Kanda, T; Masuzaki, R; Moriyama, M; Omata, M, 2020) |
| "As a subgroup of nonalcoholic fatty liver disease (NAFLD), patients with non-obese NAFLD may also have an increased risk of adverse hepatic and metabolic outcomes." | 2.66 | Epidemiology of nonalcoholic fatty liver disease in non-obese populations: Meta-analytic assessment of its prevalence, genetic, metabolic, and histological profiles. ( Fan, JG; Wong, VW; Zou, ZY, 2020) |
| "nonalcoholic fatty liver disease (NAFLD) comprises a broad spectrum of diseases, which can progress from benign steatosis to nonalcoholic steatohepatitis, liver cirrhosis and hepatocellular carcinoma." | 2.66 | Genetics and epigenetics purpose in nonalcoholic fatty liver disease. ( Botello-Manilla, AE; Chávez-Tapia, NC; Nuño-Lámbarri, N; Uribe, M, 2020) |
| "Nonalcoholic fatty liver disease (NAFLD) is one of the most common causes of chronic liver disease worldwide." | 2.66 | Association of PNPLA3 rs738409 G/C gene polymorphism with nonalcoholic fatty liver disease in children: a meta-analysis. ( Fan, ZP; Guo, HQ; Liang, S; Lin, W; Liu, YL; Liu, YR; Ma, LX; Mei, TT; Qiu, LX; Tang, S; Wei, XH; Yu, HB; Zhang, J; Zhang, WY, 2020) |
| "Both environmental factors and genetic predisposition contribute to the risk." | 2.66 | Nutrients, Genetic Factors, and Their Interaction in Non-Alcoholic Fatty Liver Disease and Cardiovascular Disease. ( Fargion, S; Fracanzani, AL; Iuculano, F; Lombardi, R; Pallini, G, 2020) |
| "Nonalcoholic fatty liver disease (NAFLD), together with metabolic syndrome and obesity, has shown a rapid increase in prevalence worldwide and is emerging as a major cause of chronic liver disease and liver transplantation." | 2.61 | Recent research trends and updates on nonalcoholic fatty liver disease. ( Cho, YK; Jun, DW; Kim, MY; Kim, SG; Kim, W; Lee, JW; Park, SH; Sohn, JH; Yeon, JE; Yoo, JJ, 2019) |
| "In some patients with NAFLD, isolated steatosis can progress to advanced stages with non-alcoholic steatohepatitis (NASH) and fibrosis, increasing the risk of cirrhosis and hepatocellular carcinoma." | 2.61 | Non-alcoholic fatty liver disease: causes, diagnosis, cardiometabolic consequences, and treatment strategies. ( Cusi, K; Häring, HU; Stefan, N, 2019) |
| "In addition, nonalcoholic steatohepatitis (NASH) was more frequently observed in G allele carriers (GG vs CC, OR = 3." | 2.61 | Association between PNPLA3 rs738409 polymorphism and nonalcoholic fatty liver disease (NAFLD) susceptibility and severity: A meta-analysis. ( Dai, G; He, S; Li, X; Liu, P; Zhou, X, 2019) |
| "First described in 1980, nonalcoholic fatty liver disease (NAFLD) has become more common although the exact incidence and prevalence is unknown." | 2.58 | NAFLD-NASH: An Under-Recognized Epidemic. ( Faselis, C; Jennings, J; Yao, MD, 2018) |
| "Nonalcoholic fatty liver disease (NAFLD) and metabolic syndrome (MS) are highly prevalent, affecting approximately one-third of the US population." | 2.58 | Nonalcoholic Fatty Liver Disease and Metabolic Syndrome. ( Kim, D; Kim, WR; Touros, A, 2018) |
| "Posttransplant metabolic syndrome is a common occurrence that increases the risk of steatosis in the graft liver." | 2.58 | Nonalcoholic Fatty Liver Disease/Nonalcoholic Steatohepatitis in Liver Transplantation. ( Carter, D; Chang, C; Dieterich, DT, 2018) |
| "Nonalcoholic fatty liver disease (NAFLD) is the leading cause of chronic liver disease in children." | 2.58 | The Genetics of Pediatric Nonalcoholic Fatty Liver Disease. ( Goyal, NP; Schwimmer, JB, 2018) |
| "Nonalcoholic fatty liver disease is emerging as the most common cause of chronic liver disease worldwide." | 2.58 | Risk Factors for the Development of Nonalcoholic Fatty Liver Disease/Nonalcoholic Steatohepatitis, Including Genetics. ( Bernstein, DE; Lim, HW, 2018) |
| "Nonalcoholic fatty liver disease (NAFLD) is the most prevalent chronic liver disease worldwide." | 2.58 | The genetic backgrounds in nonalcoholic fatty liver disease. ( Itoh, Y; Seko, Y; Yamaguchi, K, 2018) |
| "Both ARLD and NAFLD are multifactorial and refer to a spectrum of disease severity, ranging from steatosis through steatohepatitis to fibrosis and cirrhosis." | 2.58 | Genetics of alcoholic liver disease and non-alcoholic steatohepatitis. ( Anstee, QM; Scott, E, 2018) |
| "Nonalcoholic fatty liver disease (NAFLD), now the leading cause of liver damage worldwide, is epidemiologically associated with obesity, insulin resistance and type 2 diabetes, and is a potentially progressive condition to advanced liver fibrosis and hepatocellular carcinoma." | 2.58 | Genetics of Nonalcoholic Fatty Liver Disease: A 2018 Update. ( Baselli, GA; Valenti, LVC, 2018) |
| "Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease, and its detection in the general population has reached a global scale." | 2.58 | Clinical-morphological parallels of the PNPLA3 gene polymorphism in patients with nonalcoholic fatty liver disease. ( Baykova, IE; Kislyakov, VA; Nikitin, IG; Tikhomirova, AS, 2018) |
| "Currently, the population prevalence of NAFLD in Asia is around 25%, like many Western countries." | 2.55 | New trends on obesity and NAFLD in Asia. ( Fan, JG; Kim, SU; Wong, VW, 2017) |
| "Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease in the world." | 2.55 | Role of nutrition, gene polymorphism, and gut microbiota in non-alcoholic fatty liver disease. ( Kong, L; Lu, Y; Nan, Y; Qiao, L; Zhang, S, 2017) |
| "Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of metabolic syndrome and is a spectrum of conditions ranging from benign hepatic steatosis to non-alcoholic steatohepatitis (NASH); it may progress to cirrhosis and liver cancer." | 2.55 | Disturbed Vitamin A Metabolism in Non-Alcoholic Fatty Liver Disease (NAFLD). ( Blokzijl, H; Dullaart, RPF; Faber, KN; Saeed, A; Schreuder, TCMA, 2017) |
| "Insights into the topic of the genetic susceptibility in lean individuals with NAFLD and the potential use of genetic tests in identifying individuals at risk are also discussed." | 2.55 | Genetic predisposition in nonalcoholic fatty liver disease. ( Pirola, CJ; Sookoian, S, 2017) |
| "Non-alcoholic fatty liver disease (NAFLD) represents a wide spectrum of liver disease from simple steatosis, to steatohepatitis, (both with and without liver fibrosis), cirrhosis and end-stage liver failure." | 2.53 | Bidirectional Relationships and Disconnects between NAFLD and Features of the Metabolic Syndrome. ( Byrne, CD; Wainwright, P, 2016) |
| "Nonalcoholic fatty liver disease (NAFLD) is emerging as the most common cause of liver disease in the United States." | 2.53 | The Prevalence and Pathobiology of Nonalcoholic Fatty Liver Disease in Patients of Different Races or Ethnicities. ( Gaglio, PJ; Kalia, HS, 2016) |
| "Non-alcoholic fatty liver disease (NAFLD) increases risk of mortality from liver and cardiovascular disease (CVD) and is the major cause of hepatocellular carcinoma (HCC), which may develop without cirrhosis." | 2.53 | Diagnosis of non-alcoholic fatty liver disease (NAFLD). ( Yki-Järvinen, H, 2016) |
| "Non-alcoholic fatty liver disease (NAFLD) covers a spectrum of disease ranging from simple steatosis (NAFL) to non-alcoholic steatohepatitis (NASH) and fibrosis." | 2.53 | Definitions of Normal Liver Fat and the Association of Insulin Sensitivity with Acquired and Genetic NAFLD-A Systematic Review. ( Petäjä, EM; Yki-Järvinen, H, 2016) |
| "Nonalcoholic fatty liver disease (NAFLD) is a raising liver disease with increasing prevalence due to the epidemics of obesity and diabetes, with end points in cirrhosis or hepatocellular carcinoma." | 2.53 | Pharmacogenomic and personalized approaches to tackle nonalcoholic fatty liver disease. ( Lorbek, G; Rozman, D; Urlep, Ž, 2016) |
| "Non-alcoholic fatty liver disease (NAFLD) covers a spectrum of liver disease from simple steatosis to non-alcoholic steatohepatitis (NASH) and cirrhosis." | 2.53 | Non-alcoholic fatty liver disease and risk of type 2 diabetes. ( Lallukka, S; Yki-Järvinen, H, 2016) |
| "While our principal focus is on NAFLD, we also discuss briefly effects of some of the variants on development and severity of other hepatic diseases, including hepatitis C and alcoholic liver disease." | 2.53 | Genetic factors that affect nonalcoholic fatty liver disease: A systematic clinical review. ( Besur, S; Bonkovsky, HL; Severson, TJ, 2016) |
| "Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in the United States and represents an increasingly important etiology of hepatocellular carcinoma (HCC) with annual cumulative incidence rates ranging from 2% to 12% in cohorts of NAFLD cirrhosis." | 2.53 | Hepatocellular carcinoma in patients with non-alcoholic fatty liver disease. ( Lim, JK; Nguyen, MH; Wong, CR, 2016) |
| "The prevalence of Type 2 diabetes is expected to increase in parallel with obesity rates and the ageing population." | 2.52 | Practical approach to non-alcoholic fatty liver disease in patients with diabetes. ( Alazawi, W; Syn, WK; Tai, FW, 2015) |
| "Nonalcoholic fatty liver disease (NAFLD) is increasingly being diagnosed worldwide and is strongly associated with the features of metabolic syndrome." | 2.52 | A Perspective on Metabolic Syndrome and Nonalcoholic Fatty Liver Disease. ( Byrne, CD; Targher, G, 2015) |
| "Nonalcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome and comprises a liver disease spectrum ranging from steatosis to nonalcoholic steatohepatitis (NASH) with risk of progression to liver cirrhosis and hepatocellular carcinoma (HCC)." | 2.52 | Challenges and Management of Liver Cirrhosis: Practical Issues in the Therapy of Patients with Cirrhosis due to NAFLD and NASH. ( Halilbasic, E; Hofer, H; Kazemi-Shirazi, L; Kienbacher, C; Munda, P; Rechling, C; Trauner, M; Traussnigg, S, 2015) |
| "Nonalcoholic fatty liver disease (NAFLD) encompasses a spectrum that spans simple steatosis, through nonalcoholic steatohepatitis (NASH) to fibrosis and ultimately cirrhosis." | 2.52 | The Genetics of Nonalcoholic Fatty Liver Disease: Spotlight on PNPLA3 and TM6SF2. ( Anstee, QM; Day, CP, 2015) |
| "Nonalcoholic fatty liver disease (NAFLD) is caused by hepatic steatosis, which can progress to nonalcoholic steatohepatitis, fibrosis/cirrhosis, and hepatocellular carcinoma in the absence of excessive alcohol consumption." | 2.52 | Insights from Genome-Wide Association Analyses of Nonalcoholic Fatty Liver Disease. ( Halligan, B; Kahali, B; Speliotes, EK, 2015) |
| "Obesity is strongly associated with the prevalence of nonalcoholic fatty liver disease (NAFLD) in adult and pediatric populations." | 2.50 | Obesity-associated nonalcoholic fatty liver disease. ( Yilmaz, Y; Younossi, ZM, 2014) |
| "Nonalcoholic fatty liver disease (NAFLD) is a complex disease." | 2.50 | Host genetic variants in obesity-related nonalcoholic fatty liver disease. ( Birerdinc, A; Mehta, R; Younossi, ZM, 2014) |
| "Metabolic syndrome is a cluster of metabolic abnormalities that identifies people at risk of diabetes and cardiovascular disease, whereas non-alcoholic fatty liver disease (NAFLD) is defined as a disorder with excess fat in the liver due to non-alcoholic causes." | 2.50 | Non-alcoholic fatty liver disease as a cause and a consequence of metabolic syndrome. ( Yki-Järvinen, H, 2014) |
| "Non-alcoholic fatty liver disease (NAFLD) is a chronic liver disease that might affect up to one-third of the adult population in industrialised countries." | 2.50 | Non-alcoholic fatty liver disease and type 2 diabetes mellitus: the liver disease of our age? ( Firneisz, G, 2014) |
| "Although the mechanisms underlying disease progression are incompletely understood, lipotoxic events in the liver resulting in inflammation and fibrosis appear to be central." | 2.50 | Role of metabolic lipases and lipolytic metabolites in the pathogenesis of NAFLD. ( Claudel, T; Fuchs, CD; Trauner, M, 2014) |
| "Nonalcoholic fatty liver disease (NAFLD) is an obesity-related condition affecting over 50% of individuals in some populations and is expected to become the number one cause of liver disease worldwide by 2020." | 2.49 | Characterization of European ancestry nonalcoholic fatty liver disease-associated variants in individuals of African and Hispanic descent. ( Bielak, LF; Borecki, IB; Carr, JJ; Feitosa, MF; Harris, TB; Hernaez, R; Jhun, MA; Kahali, B; Kardia, SL; Langefeld, CD; Liu, J; Mosley, TH; Musani, SK; Norris, JM; Palmer, ND; Peyser, PA; Smith, AV; Speliotes, EK; Taylor, HA; Wagenknecht, LE; Yerges-Armstrong, LM, 2013) |
| "As such, NAFLD is best considered a complex disease trait resulting from environmental exposures acting on a susceptible polygenic background and comprising multiple independent modifiers." | 2.49 | The genetics of NAFLD. ( Anstee, QM; Day, CP, 2013) |
| "Nonalcoholic fatty liver disease is one of the most common hepatic disorders worldwide." | 2.49 | PNPLA3-associated steatohepatitis: toward a gene-based classification of fatty liver disease. ( Krawczyk, M; Lammert, F; Portincasa, P, 2013) |
| "Nonalcoholic steatohepatitis (NASH) was more frequently observed in GG than CC homozygous (odds ratio [OR] 3." | 2.47 | Meta-analysis of the influence of I148M variant of patatin-like phospholipase domain containing 3 gene (PNPLA3) on the susceptibility and histological severity of nonalcoholic fatty liver disease. ( Pirola, CJ; Sookoian, S, 2011) |
| "Nonalcoholic fatty liver disease (NAFLD) clusters in families, but the only known common genetic variants influencing risk are near PNPLA3." | 2.47 | Genome-wide association analysis identifies variants associated with nonalcoholic fatty liver disease that have distinct effects on metabolic traits. ( Borecki, IB; Butler, JL; Carr, JJ; Clark, JM; Eiriksdottir, G; Feitosa, MF; Fox, CS; Garcia, ME; Gudnason, V; Harris, TB; Hernaez, R; Hirschhorn, JN; Hoffmann, U; Hwang, SJ; Kao, WH; Kim, LJ; Launer, LJ; Massaro, JM; Mitchell, BD; Nalls, MA; O'Donnell, CJ; Palmer, CD; Sahani, DV; Salomaa, V; Schadt, EE; Schwartz, SM; Shuldiner, AR; Siscovick, DS; Smith, AV; Speliotes, EK; Tomas, M; Voight, BF; Wu, J; Yerges-Armstrong, LM, 2011) |
| "Nonalcoholic fatty liver disease (NAFLD) in most patients involves only simple hepatic steatosis; however, a minority develop progressive steatohepatitis." | 2.47 | Genetic determinants of susceptibility and severity in nonalcoholic fatty liver disease. ( Ballestri, S; Carulli, L; Daly, AK; Day, CP; Loria, P, 2011) |
| "We included 228 patients with NAFLD (body mass index-Z [BMI-Z] = 2." | 1.72 | Effects of PNPLA3, TM6SF2 and SAMM50 on the development and severity of non-alcoholic fatty liver disease in children. ( Kim, NY; Ko, JS; Lee, KJ; Moon, JS, 2022) |
| "Non-alcoholic fatty liver disease (NAFLD) is closely associated with metabolic dysfunction." | 1.72 | Protective association of Klotho rs495392 gene polymorphism against hepatic steatosis in non-alcoholic fatty liver disease patients. ( de Knegt, RJ; Ghanbari, M; Li, G; Liu, WY; Ma, HL; Pan, Q; Rios, RS; Tang, LJ; Valenti, L; Wang, XD; Zhang, X; Zheng, KI; Zheng, MH; Zhu, PW, 2022) |
| "To investigate the effects of the NAFLD risk alleles on the all-cause and cause-specific mortality in 5581 Chinese adults." | 1.72 | NAFLD-related gene polymorphisms and all-cause and cause-specific mortality in an Asian population: the Shanghai Changfeng Study. ( Aleteng, Q; Chen, L; Gao, X; Ge, J; He, W; Hu, Y; Huang, Q; Li, Q; Li, X; Lin, H; Ma, H; Ma, S; Pan, B; Tang, H; Wang, S; Wu, L; Wu, Q; Xia, M; Xu, W; Zeng, H; Zheng, Y, 2022) |
| "Three hundred and fifty seven NAFLD patients were enrolled, all previously instructed to follow a Mediterranean diet (MD)." | 1.72 | Interaction between Lifestyle Changes and PNPLA3 Genotype in NAFLD Patients during the COVID-19 Lockdown. ( Alletto, F; Bertelli, C; Cespiati, A; Cinque, F; Colavolpe, L; Costantino, A; Dongiovanni, P; Fargion, S; Fatta, E; Fracanzani, AL; Francione, P; Lombardi, R; Maffi, G; Oberti, G; Sigon, G; Vecchi, M, 2022) |
| "In nonalcoholic fatty liver disease (NAFLD) the patatin-like phospholipase domain-containing 3 (PNPLA3) rs738409 variant is a contributor." | 1.72 | Hepatic patatin-like phospholipase domain-containing 3 levels are increased in I148M risk allele carriers and correlate with NAFLD in humans. ( Andréasson, AC; Antonsson, M; Bergenholm, L; Carlsson, B; Dix, CI; Ekstedt, M; Ericson, E; Fjellström, O; Hansson, SF; Kechagias, S; Knöchel, J; Lee, R; Liljeblad, M; Lindén, D; Nasr, P; Schumi, J, 2022) |
| "Non-alcoholic fatty liver disease (NAFLD) shares several risk factors with atherosclerosis, as it is associated with components of the metabolic syndrome." | 1.72 | Association of rs738409 Polymorphism in Adiponutrin Gene with Liver Steatosis and Atherosclerosis Risk Factors in Greek Children and Adolescents. ( Emmanouilidou-Fotoulaki, E; Fotoulaki, M; Kavga, M; Lambropoulos, AF; Papadopoulou-Legbelou, K; Sotiriadou, F; Stasinou, E, 2022) |
| "Advanced fibrosis was diagnosed by liver biopsy or elastography." | 1.72 | Effect of common genetic variants on the risk of cirrhosis in non-alcoholic fatty liver disease during 20 years of follow-up. ( Ekstedt, M; Hagström, H; Holmer, M; Kechagias, S; Nasr, P; Romeo, S; Stål, P; Tavaglione, F; Wester, A; Zenlander, R, 2022) |
| "Nonalcoholic fatty liver disease (NAFLD) has become the most common chronic liver disease in children and adolescents, increasing the risk of its progression toward nonalcoholic steatohepatitis (NASH), cirrhosis, and cancer." | 1.72 | Profiling of cell-free DNA methylation and histone signatures in pediatric NAFLD: A pilot study. ( Alisi, A; Balsano, C; Bianco, SD; Braghini, MR; Buzova, D; Cerveny, J; Crudele, A; Frohlich, J; Kisheva, A; Lo Re, O; Mazza, T; Mosca, A; Raffaele, M; Sartorelli, MR; Vinciguerra, M, 2022) |
| "Among subjects with NAFLD in the Boramae cohort, the G allele was independently associated with a lower prevalence of DM in both NAFL (odds ratio [OR] per 1 allele, 0." | 1.72 | A PNPLA3 Polymorphism Confers Lower Susceptibility to Incident Diabetes Mellitus in Subjects With Nonalcoholic Fatty Liver Disease. ( Chang, MS; Chung, GE; Joo, SK; Kim, W; Koo, BK; Moon, S; Park, JH; Yoon, JW, 2022) |
| "Nonalcoholic fatty liver disease (NAFLD), insulin resistance and liver fibrosis are prevalent in individuals co-infected with HIV type 1 (HIV-1)/hepatitis C virus (HCV), even after HCV eradication." | 1.62 | Single nucleotide polymorphisms in PNPLA3, ADAR-1 and IFIH1 are associated with advanced liver fibrosis in patients co-infected with HIV-1//hepatitis C virus. ( Bechini, J; Clotet, B; de Cid, R; Franco, S; Galván-Femenía, I; Horneros, J; Llibre, JM; Martínez, MA; Ouchi, D; Perez, R; Soldevila, L; Tenesa, M; Tural, C, 2021) |
| "Many patients with nonalcoholic fatty liver disease (NAFLD) also have diabetes." | 1.62 | Development and course of diabetes according to genetic factors and diabetes treatment among patients with nonalcoholic fatty liver disease. ( Hashimoto, E; Kodama, K; Kogiso, T; Sagawa, T; Taniai, M; Tokushige, K, 2021) |
| "Obesity is closely associated with non-alcoholic fatty liver disease (NAFLD), and elevated serum palmitate is the link between obesity and excessive hepatic lipid accumulation." | 1.62 | Palmitate induces fat accumulation via repressing FoxO1-mediated ATGL-dependent lipolysis in HepG2 hepatocytes. ( Cheng, Y; Feng, Y; Han, L; Li, T; Liu, X; Tan, H; Wang, L; Zhao, N, 2021) |
| "We enrolled 655 NAFLD patients and 504 controls." | 1.62 | Mitochondrial haplogroup G is associated with nonalcoholic fatty liver disease, while haplogroup A mitigates the effects of PNPLA3. ( Chen, J; Gusdon, AM; Hui, Y; Mathews, CE; Qu, S, 2021) |
| "The histological spectrum of NAFLD was classified according to the NASH clinical research network scoring system." | 1.62 | Individualized Polygenic Risk Score Identifies NASH in the Eastern Asia Region: A Derivation and Validation Study. ( Byrne, CD; Chen, SD; Chen, YP; Gao, F; Kim, W; Lee, DH; Targher, G; Wang, XD; Wu, XX; Zheng, KI; Zheng, MH, 2021) |
| "Non-alcoholic fatty liver disease (NAFLD) is a global health burden." | 1.62 | Combined analysis of gut microbiota, diet and PNPLA3 polymorphism in biopsy-proven non-alcoholic fatty liver disease. ( Demir, M; Farowski, F; Goeser, T; J G T Vehreschild, M; Kasper, P; Krawczyk, M; Kretzschmar, A; Lammert, F; Lang, S; Martin, A; Mohr, R; Nowag, A; Roderburg, C; Schnabl, B; Scholz, C; Steffen, HM; Tacke, F; Wisplinghoff, H; Zhang, X, 2021) |
| "Non-alcoholic fatty liver disease (NAFLD) is a chronic metabolic liver disease associated with obesity and insulin resistance." | 1.62 | P2Y2R Deficiency Ameliorates Hepatic Steatosis by Reducing Lipogenesis and Enhancing Fatty Acid β-Oxidation through AMPK and PGC-1α Induction in High-Fat Diet-Fed Mice. ( Dusabimana, T; Je, J; Jeong, K; Kim, H; Kim, HJ; Park, EJ; Park, SW; Yun, SP, 2021) |
| "Patients with biopsy-proven NAFLD were genotyped for the PNPLA3-rs738409(minor allele:G), TM6SF2-rs58542926(minor allele:T) and HSD17B13- rs72613567 (minor allele:TA) variants." | 1.62 | Combined effects of PNPLA3, TM6SF2 and HSD17B13 variants on severity of biopsy-proven non-alcoholic fatty liver disease. ( Aigner, E; Buch, S; Canbay, A; Datz, C; Ferenci, P; Halilbasic, E; Hampe, J; Keritam, O; Mandorfer, M; Meyer, EL; Munda, P; Paternostro, R; Prager, G; Schafmayer, C; Schlattjan, M; Sipos, B; Stättermayer, AF; Staufer, K; Stickel, F; Stift, J; Trauner, M; Traussnigg, S; Wrba, F, 2021) |
| "Non-alcoholic fatty liver disease (NAFLD) is the fastest growing cause of chronic liver disease worldwide." | 1.62 | Natural history of NASH. ( Armandi, A; Bugianesi, E, 2021) |
| "However, the pathogenesis of NAFLD has not yet been fully elucidated, and the importance of genetic factors has only recently been appreciated." | 1.62 | Modeling PNPLA3-Associated NAFLD Using Human-Induced Pluripotent Stem Cells. ( Hu, Z; Jenkins, B; Koulman, A; Lenaerts, AS; Liang, TJ; Morell, CM; Park, SB; Tilson, SG; Vallier, L, 2021) |
| "Thirty-seven patients with NAFLD had NASH, of which 12 were nonobese." | 1.62 | PPARGC1A rs8192678 G>A polymorphism affects the severity of hepatic histological features and nonalcoholic steatohepatitis in patients with nonalcoholic fatty liver disease. ( Cao, HX; Chen, GY; Fan, JG; Pan, Q; Shen, F; Zhang, RN, 2021) |
| "Patients with nonalcoholic fatty liver disease (NAFLD) have an increased risk for liver-related complications, such as decompensation, hepatocellular carcinoma (HCC), and death; the severity of liver fibrosis and metabolic comorbidities are the main risk factors." | 1.56 | Association Between PNPLA3 rs738409 C>G Variant and Liver-Related Outcomes in Patients With Nonalcoholic Fatty Liver Disease. ( Barcellona, MR; Boemi, R; Cammà, C; Celsa, C; Craxì, A; Di Marco, V; Enea, M; Giannetti, A; Grimaudo, S; Marchesini, G; Pennisi, G; Petta, S; Pipitone, RM; Spatola, F, 2020) |
| "Patients with NAFLD and persistently nALT, who carry the PNPLA3 rs738409 G allele, are at higher risk of early glomerular and tubular damage." | 1.56 | PNPLA3 rs738409 is associated with renal glomerular and tubular injury in NAFLD patients with persistently normal ALT levels. ( Byrne, CD; Chen, YP; Ma, HL; Pan, XY; Sun, DQ; Targher, G; Wang, XD; Xu, G; Yuan, WJ; Zhang, HY; Zheng, KI; Zheng, MH; Zhu, PW, 2020) |
| "Nonalcoholic fatty liver disease (NAFLD) and chronic kidney disease (CKD) share risk factors, and recent meta-analysis confirmed that NAFLD is an independent risk factor for incident CKD." | 1.56 | Association Between a Polymorphism in MBOAT7 and Chronic Kidney Disease in Patients With Biopsy-Confirmed Nonalcoholic Fatty Liver Disease. ( An, JN; Bae, JM; Chang, MS; Joo, SK; Kim, D; Kim, JH; Kim, W; Koo, BK; Lee, S; Park, JH, 2020) |
| "population, PNPLA3 I148M and higher NAFLD liver fat and fibrosis scores were associated with increased liver disease mortality." | 1.56 | Patatin-Like Phospholipase Domain-Containing Protein 3 I148M and Liver Fat and Fibrosis Scores Predict Liver Disease Mortality in the U.S. Population. ( Ruhl, CE; Unalp-Arida, A, 2020) |
| "NAFLD was defined by ultrasound detected liver steatosis and/or ALT > 40 IU/L." | 1.56 | Transmembrane 6 superfamily member 2 167K allele improves renal function in children with obesity. ( Cirillo, G; Di Sessa, A; Guarino, S; La Manna, A; Marzuillo, P; Miraglia Del Giudice, E; Pedullà, M; Umano, GR, 2020) |
| "Non-alcoholic fatty liver disease (NAFLD) is commonly diagnosed in patients presenting with metabolic syndrome (MetS) and has been associated with single nucleotide polymorphisms of rs738409 in the patatin-like phospholipase domain containing 3 (PNPLA3) gene." | 1.56 | Association of metabolic syndrome and patatin-like phospholipase 3 - rs738409 gene variant in non-alcoholic fatty liver disease among a Chennai-based south Indian population. ( Karthick, R; Mohan, N; Narayanasamy, K; Panneerselvam, P; Prakash, R; Rajaram, M; Ramachandran, A, 2020) |
| "'Severe NAFLD' was defined as the presence of steatohepatitis, NAFLD activity score ≥4 or fibrosis stage ≥2." | 1.56 | Liver transcriptomics highlights interleukin-32 as novel NAFLD-related cytokine and candidate biomarker. ( Badiali, S; Baselli, GA; Dongiovanni, P; Fracanzani, AL; Maggioni, M; Mancina, RM; Maurotti, S; Meroni, M; Montalcini, T; Pelusi, S; Pingitore, P; Prati, D; Rametta, R; Romeo, S; Rossi, G; Taliento, AE; Valenti, L, 2020) |
| "There are no biomarkers of nonalcoholic steatohepatitis (NASH) that are ready for routine clinical use." | 1.56 | Development and Validation of a Scoring System, Based on Genetic and Clinical Factors, to Determine Risk of Steatohepatitis in Asian Patients with Nonalcoholic Fatty Liver Disease. ( Bae, JM; Chang, MS; Joo, SK; Kim, D; Kim, JH; Kim, W; Koo, BK; Lee, S; Park, JH, 2020) |
| "non-carriers; ii) increased NAFLD risk (odds ratio 1." | 1.56 | A common variant in PNPLA3 is associated with age at diagnosis of NAFLD in patients from a multi-ethnic biobank. ( Abul-Husn, NS; Belbin, GM; Cho, J; Gignoux, CR; Kenny, EE; Loos, RJF; Moscati, A; Nadkarni, G; Sorokin, EP; Van Vleck, T; Walker, RW; Wojcik, GL, 2020) |
| "Non-alcoholic fatty liver disease (NAFLD), type 2 diabetes (T2D) and obesity are epidemiologically correlated with each other but the causal inter-relationships between them remain incompletely understood." | 1.56 | Causal relationships between NAFLD, T2D and obesity have implications for disease subphenotyping. ( Cai, D; Chen, YE; Dong, XC; Graham, S; Huang, M; Liu, W; Liu, Z; Pique-Regi, R; Wang, X; Willer, C; Zhang, Y, 2020) |
| "Fibrosis progression in autoimmune hepatitis can be attenuated by immunosuppressive treatment; however, some patients progress despite therapy." | 1.56 | The PNPLA3 rs738409 GG genotype is associated with poorer prognosis in 239 patients with autoimmune hepatitis. ( Großhennig, A; Kirstein, MM; Manns, MP; Marhenke, S; Mederacke, I; Mederacke, YS; Metzler, F; Vogel, A, 2020) |
| "Non-alcoholic fatty liver disease (NAFLD) is often associated with metabolic syndrome (type 2 diabetes, hypertension, hypertriglyceridemia, insulin resistance, and obesity)." | 1.56 | The effect of PNPLA3 polymorphism as gain in function mutation in the pathogenesis of non-alcoholic fatty liver disease. ( Akkız, H; Delik, A; Dinçer, S, 2020) |
| "In Japanese patients with NAFLD, carriage of the HSD17B13 rs6834314 G allele attenuated the effect of the PNPLA3 rs738409 GG genotype on advanced hepatic fibrosis." | 1.56 | Attenuated effect of PNPLA3 on hepatic fibrosis by HSD17B13 in Japanese patients with non-alcoholic fatty liver disease. ( Itoh, Y; Kataoka, S; Mori, K; Moriguchi, M; Okanoue, T; Okishio, S; Okuda, K; Seko, Y; Takahashi, A; Tanaka, S; Tochiki, N; Umemura, A; Yamaguchi, K; Yano, K, 2020) |
| "Despite this, the genetic susceptibility to chronic liver disease in this country has not been investigated." | 1.56 | Genetic Susceptibility to Chronic Liver Disease in Individuals from Pakistan. ( Ahmad, IN; Ciociola, E; Dar, FS; Kaukab Raja, G; Mancina, RM; Moaeen-Ud-Din, M; Naqvi, SMS; Raja, AM; Romeo, S, 2020) |
| "Yale Pediatric Obesity Clinic." | 1.56 | Effect of Gut Microbiota and PNPLA3 rs738409 Variant on Nonalcoholic Fatty Liver Disease (NAFLD) in Obese Youth. ( Feinn, R; Galuppo, B; Graf, J; Monga Kravetz, A; Pierpont, B; Santoro, N; Siebel, S; Testerman, T, 2020) |
| "Nonalcoholic fatty liver disease (NAFLD) has been associated with greater cerebral white matter hyperintensity (WMH) volume and microbleeds." | 1.56 | Association between PNPLA3 rs738409 G variant and MRI cerebrovascular disease biomarkers. ( Del Brutto, VJ; Dueker, N; Elkind, MSV; Gutierrez, J; Parikh, NS; Rundek, T; Sacco, RL; Varela, D; Wright, CB, 2020) |
| "Genetic variants spanning eight NAFLD risk or ALT-associated loci (LYPLAL1, GCKR, HSD17B13, TRIB1, PPP1R3B, ERLIN1, TM6SF2, PNPLA3) were tested for NAFLD associations with sensitivity analyses adjusting for metabolic risk factors and alcohol consumption." | 1.56 | Validating a non-invasive, ALT-based non-alcoholic fatty liver phenotype in the million veteran program. ( Assimes, TL; Carr, RM; Chang, KM; Damrauer, SM; DuVall, SL; Gaziano, JM; Justice, AC; Kaplan, DE; Kranzler, HR; Lee, JS; Lee, KM; Lynch, JA; Meigs, JB; Miller, DR; Muralidhar, S; O'Donnell, CJ; Phillips, LS; Pyarajan, S; Rader, DJ; Reaven, PD; Saleheen, D; Serper, M; Shao, Q; Tsao, PS; Vickers-Smith, R; Voight, BF; Vujkovic, M; Wilson, PWF, 2020) |
| "PNPLA3 I148M might modify the anti-NAFLD response to exenatide." | 1.56 | PNPLA3 I148M is involved in the variability in anti-NAFLD response to exenatide. ( Chen, Y; Liang, H; Xu, F; Xu, X; Yan, X; Yuan, S, 2020) |
| "Non-alcoholic fatty liver disease (NAFLD) is a common chronic condition caused by the accumulation of fat in the liver." | 1.56 | Validating candidate biomarkers for different stages of non-alcoholic fatty liver disease. ( Al-Otaibi, M; Al-Qarni, R; Al-Saif, F; Alfadda, AA; Alkhalidi, H; Bamehriz, F; Hassanain, M; Iqbal, M, 2020) |
| "NAFLD was defined by ultrasound detected liver steatosis and/or alanine aminotransferase (ALT) levels > 40 IU/L." | 1.56 | Pediatric non-alcoholic fatty liver disease and kidney function: Effect of ( Cirillo, G; Cozzolino, D; Di Sessa, A; Guarino, S; Marzuillo, P; Miraglia Del Giudice, E; Passaro, AP; Umano, GR; Verde, V, 2020) |
| "Nonalcoholic fatty liver disease (NAFLD) is characterized by hepatic lipid accumulation." | 1.56 | Effects of TM6SF2 E167K on hepatic lipid and very low-density lipoprotein metabolism in humans. ( Adiels, M; Björnson, E; Borén, J; Hakkarainen, A; Mancina, RM; Matikainen, N; Packard, CJ; Palotie, A; Rämö, J; Ripatti, P; Ripatti, S; Romeo, S; Söderlund, S; Ståhlman, M; Taskinen, MR, 2020) |
| "Although the presence of nonalcoholic fatty liver disease (NAFLD) is known to be related to subclinical atherosclerosis, the relationship between the severity of NAFLD and subclinical atherosclerosis is not clear." | 1.51 | Factors influencing subclinical atherosclerosis in patients with biopsy-proven nonalcoholic fatty liver disease. ( Arai, T; Atsukawa, M; Emoto, N; Hatori, T; Hayama, K; Iio, E; Itokawa, N; Iwakiri, K; Iwashita, A; Kaneko, K; Kawamoto, C; Kawano, T; Koeda, M; Kondo, C; Okubo, T; Tanabe, T; Tanaka, Y; Tsubota, A; Yoshida, Y, 2019) |
| "Nonalcoholic fatty liver disease (NAFLD) is closely associated with obesity and insulin resistance, and therefore predisposes to type 2 diabetes and cardiovascular diseases." | 1.51 | PNPLA3 I148M Polymorphism in Patients with Nonalcoholic Fatty Liver Disease, Obesity and Prediabetes. ( Alexiev, A; Assyov, Y; Gateva, A; Ivanova, I; Ivanova, R; Ivanova-Boyanova, R; Kamenov, Z; Karamfilova, V; Mateva, L; Savov, A; Vlahova, Z; Yaneva, N, 2019) |
| "Non-alcoholic fatty liver disease (NAFLD) is associated with chronic kidney disease (CKD)." | 1.51 | FIB-4 Index and Diabetes Mellitus Are Associated with Chronic Kidney Disease in Japanese Patients with Non-Alcoholic Fatty Liver Disease. ( Itoh, Y; Kataoka, S; Mizuno, N; Moriguchi, M; Nishikawa, T; Okanoue, T; Okishio, S; Okuda, K; Seko, Y; Takahashi, A; Takemura, M; Taketani, H; Umemura, A; Yamaguchi, K; Yano, K, 2019) |
| "Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in children and adolescents today." | 1.51 | Genetic determinants of steatosis and fibrosis progression in paediatric non-alcoholic fatty liver disease. ( Berndt, N; Bläker, H; Bufler, P; Cadenas, C; Golka, K; Hengstler, JG; Henning, S; Holzhütter, HG; Hudert, CA; Jansen, PLM; Loddenkemper, C; Meierhofer, D; Reinders, J; Rudolph, B; Selinski, S; Thielhorn, R; Wiegand, S, 2019) |
| "Nonalcoholic fatty liver disease (NAFLD) disproportionally affects Hispanic/Latino populations." | 1.51 | American Ancestry Is a Risk Factor for Suspected Nonalcoholic Fatty Liver Disease in Hispanic/Latino Adults. ( Cai, J; Cooper, RS; Cotler, SJ; Daviglus, M; Kallwitz, ER; Kuniholm, MH; Tayo, BO, 2019) |
| "non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disorder in the western world." | 1.51 | Comparative study of overweight and obese patients with nonalcoholic fatty liver disease. ( Aller, R; Antolín, B; Burgueño Gomez, B; de Luis Román, D; Durà, M; Fernández, N; Fernández-Rodríguez, C; García, C; Lorenzo, S; Pina, M; Sigüenza, R, 2019) |
| "Nonalcoholic fatty liver disease (NAFLD) is becoming a leading cause of advanced chronic liver disease." | 1.51 | Pnpla3 silencing with antisense oligonucleotides ameliorates nonalcoholic steatohepatitis and fibrosis in Pnpla3 I148M knock-in mice. ( Ahlstedt, I; Ahnmark, A; Åkerblad, P; Andréasson, AC; Bhanot, S; Bjursell, M; Bohlooly-Y, M; Böttcher, G; Carlsson, B; Ciociola, E; Graham, M; Haynes, WG; Lee, R; Lindblom, A; Lindén, D; Madeyski-Bengtson, K; Mancina, RM; Murray, S; Pingitore, P; Romeo, S; Sasidharan, K; Ståhlman, M; Valenti, L; Zurek, M, 2019) |
| "Non‑alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease, and has high rates of morbidity and mortality worldwide." | 1.51 | Effects of daphnetin on lipid metabolism, insulin resistance and oxidative stress in OA‑treated HepG2 cells. ( Chen, Y; Han, F; Liao, L; Liu, Y, 2019) |
| "To evaluate, in patients with nonalcoholic fatty liver disease (NAFLD), the role of lifetime exposures associated with genetic predisposition, family history (parental obesity, economic income), programming during fetal life (gestational age, birthweight), being breastfed or not, and later biomarkers of dietary habits and lifestyle in the development of fibrosis." | 1.51 | The Role of Genetic Predisposition, Programing During Fetal Life, Family Conditions, and Post-natal Diet in the Development of Pediatric Fatty Liver Disease. ( Agostoni, C; Alisi, A; De Cosmi, V; Mosca, A; Nobili, V; Parazzini, F; Raponi, M, 2019) |
| "Patients with NAFLD showed significantly lower eGFR levels compared with subjects without NAFLD." | 1.51 | Nonalcoholic fatty liver disease and eGFR levels could be linked by the PNPLA3 I148M polymorphism in children with obesity. ( Capalbo, D; Cirillo, G; Di Sessa, A; Guarino, S; La Manna, A; Marzuillo, P; Miraglia Del Giudice, E; Pedullà, M; Umano, GR, 2019) |
| "Low ASM% was inversely associated with NAFLD in PNPLA3 CC (odds ratio [OR]: men, 0." | 1.51 | The PNPLA3 rs738409 C>G variant influences the association between low skeletal muscle mass and NAFLD: the Shanghai Changfeng Study. ( Aleteng, Q; Chen, LY; Gao, J; Gao, X; He, WY; Hu, Y; Li, Q; Lin, HD; Ma, H; Wu, L; Xia, MF, 2019) |
| "Nonalcoholic fatty liver disease (NAFLD) is the commonest liver disease in children and adolescents in Western countries." | 1.51 | Contribution of a genetic risk score to clinical prediction of hepatic steatosis in obese children and adolescents. ( Byrne, CD; Corradi, M; Dauriz, M; Maffeis, C; Mantovani, A; Miraglia Del Giudice, E; Morandi, A; Olivieri, F; Targher, G; Valenti, L; Zusi, C, 2019) |
| "In the development and progression of NAFLD genetic mutations also play a significant role." | 1.51 | Association of Genetic Non-alcoholic Fatty Liver Disease with Insulin Resistance-Are we Different? ( Beg, MS; Fatima, J; Karoli, R; Khan, MA; Siddiqi, Z; Singh, PS; Varshney, S, 2019) |
| "Non-alcoholic fatty liver disease (NAFLD) is a common chronic liver illness with a genetically heterogeneous background that can be accompanied by considerable morbidity and attendant health care costs." | 1.51 | GWAS and enrichment analyses of non-alcoholic fatty liver disease identify new trait-associated genes and pathways across eMERGE Network. ( Benoit, B; Carey, DJ; Carrell, DS; Carroll, RJ; Cobb, BL; Connolly, JJ; Crosslin, DR; Divanovic, S; Gharavi, AG; Hakonarson, H; Harley, ITW; Harley, JB; Huang, Y; Jarvik, GP; Kullo, IJ; Larson, EB; Li, R; Lingren, T; Mentch, FD; Murphy, S; Namjou, B; Niu, X; Pacheco, JA; Parameswaran, S; Ritchie, MD; Stanaway, IB; Verma, S; Wei, WQ; Williams, MS; Xanthakos, SA, 2019) |
| "Genetic factors may impact nonalcoholic fatty liver disease (NAFLD) severity." | 1.51 | PNPLA3 gene polymorphism in Brazilian patients with type 2 diabetes: A prognostic marker beyond liver disease? ( Cardoso, CR; França, PH; Leite, NC; Machado, CM; Salles, GF; Villela-Nogueira, CA, 2019) |
| "The present study in 36 NAFLD patients and 27 healthy volunteers was performed." | 1.48 | Polymorphism of receptor-type tyrosine-protein phosphatase delta gene in the development of non-alcoholic fatty liver disease. ( Abe, M; Fujiya, M; Hasebe, C; Hasebe, T; Hayashi, H; Nakajima, S; Okumura, T; Sawada, K; Tanaka, H, 2018) |
| "The prevalence of PNPLA3 CG/GG in the NAFLD cohort was higher than that in the health check cohort (p < 0." | 1.48 | Combination of PNPLA3 and TLL1 polymorphism can predict advanced fibrosis in Japanese patients with nonalcoholic fatty liver disease. ( Hara, T; Itoh, Y; Kamaguchi, M; Kobayashi, M; Matsuura, K; Mizuno, N; Mochizuki, N; Mori, K; Moriguchi, M; Nishikawa, T; Nishioji, K; Okuda, K; Seko, Y; Takemura, M; Taketani, H; Tanaka, S; Tanaka, Y; Umemura, A; Yamaguchi, K; Yasui, K, 2018) |
| "The development of nonalcoholic fatty liver disease (NAFLD) is associated with multiple genetic and environmental factors." | 1.48 | Genetic Polymorphisms of PNPLA3 and SAMM50 Are Associated with Nonalcoholic Fatty Liver Disease in a Korean Population. ( Choe, EK; Chung, GE; Kim, JA; Kim, JS; Kwak, MS; Lee, JE; Lee, Y; Park, B; Yang, JI; Yim, JY, 2018) |
| "Nonalcoholic fatty liver disease is epidemiologically associated with hepatic and metabolic disorders." | 1.48 | Causal relationship of hepatic fat with liver damage and insulin resistance in nonalcoholic fatty liver. ( Badiali, S; Carlsson, LMS; Cespiati, A; Craxi, A; Dongiovanni, P; Fargion, S; Grimaudo, S; Kozlitina, J; Maggioni, M; Mancina, RM; Mannisto, V; Pelusi, S; Petta, S; Pietrelli, A; Pihlajamaki, J; Pingitore, P; Pipitone, RM; Romeo, S; Stender, S; Taube, M; Valenti, L, 2018) |
| "Non-alcoholic fatty liver disease (NAFLD) is the accumulation of extra fat in liver cells not caused by alcohol." | 1.48 | Genetic variants in COL13A1, ADIPOQ and SAMM50, in addition to the PNPLA3 gene, confer susceptibility to elevated transaminase levels in an admixed Mexican population. ( Cabrera-Álvarez, G; Canizales-Quinteros, S; Flores, YN; Larrieta-Carrasco, E; León-Mimila, P; López-Pérez, TV; Macías-Kauffer, LR; Quiterio, M; Ramírez-Palacios, P; Ramírez-Salazar, EG; Rivera-Paredez, B; Salmerón, J; Velázquez-Cruz, R; Zhang, ZF, 2018) |
| "We enrolled 189 Mexican patients with NAFLD and 201 healthy controls." | 1.48 | More Evidence for the Genetic Susceptibility of Mexican Population to Nonalcoholic Fatty Liver Disease through PNPLA3. ( Canizales-Quinteros, S; Chinchilla-López, P; Cruz-Ramón, V; Domínguez-López, A; Méndez-Sánchez, N; Ponciano-Rodríguez, G; Ramírez-Pérez, O; Sánchez-Muñoz, F, 2018) |
| "NAFLD is a polygenic condition but the individual and cumulative contribution of identified genes remains to be established." | 1.48 | Evaluation of Polygenic Determinants of Non-Alcoholic Fatty Liver Disease (NAFLD) By a Candidate Genes Resequencing Strategy. ( Angelico, F; Angeloni, A; Arca, M; Bailetti, D; Baratta, F; Belardinilli, F; Ceci, F; D'Erasmo, L; De Masi, B; Del Ben, M; Di Costanzo, A; Giannini, G; Girelli, G; Montali, A; Pastori, D; Polimeni, L; Sponziello, M, 2018) |
| "The prevalence of NAFLD in the cohort was 48%." | 1.48 | Prevalence and severity of nonalcoholic fatty liver disease by transient elastography: Genetic and metabolic risk factors in a general population. ( Buscemi, C; Buscemi, S; Craxì, A; Di Marco, V; Grimaudo, S; Petta, S; Pipitone, RM, 2018) |
| "Indirect measurement of liver fibrosis (Pediatric NAFLD Fibrosis Index [PNFI]) and a genetic risk score from these polymorphisms were calculated." | 1.48 | The Membrane-bound O-Acyltransferase7 rs641738 Variant in Pediatric Nonalcoholic Fatty Liver Disease. ( Cirillo, G; Del Giudice, EM; Del Prete, A; Di Sessa, A; Iacomino, R; Marzuillo, P; Umano, GR, 2018) |
| "The association profiles of NAFLD-risk alleles in PNPLA3, TM6SF2, GCKR, and LYPLAL1 with the corresponding metabolic measures were obtained from a publicly available metabolomics GWAS including up to 24 925 Europeans." | 1.48 | NAFLD risk alleles in PNPLA3, TM6SF2, GCKR and LYPLAL1 show divergent metabolic effects. ( Ala-Korpela, M; Kähönen, M; Kangas, AJ; Kettunen, J; Lehtimäki, T; Männikkö, M; Raitakari, OT; Sebert, S; Sliz, E; Soininen, P; Viikari, J; Würtz, P, 2018) |
| "Identifying NAFLD patients at risk of progression is crucial to orient medical care and resources." | 1.48 | Combining Genetic Variants to Improve Risk Prediction for NAFLD and Its Progression to Cirrhosis: A Proof of Concept Study. ( Antonelli-Incalzi, R; Baiocchini, A; Carotti, S; Cecere, R; De Vincentis, A; Del Nonno, F; Dell'Unto, C; Delle Monache, M; Galati, G; Gallo, P; Giannelli, V; Morini, S; Pellicelli, AM; Picardi, A; Rosati, D; Valentini, F; Vespasiani-Gentilucci, U, 2018) |
| "Non-alcoholic fatty liver disease (NAFLD) is associated with inefficient macro- and micronutrient metabolism, and alteration of circulating phospholipid compositions defines the signature of NAFLD." | 1.48 | Circulating Phospholipid Patterns in NAFLD Patients Associated with a Combination of Metabolic Risk Factors. ( Chamulitrat, W; Gan-Schreier, H; Pathil, A; Stremmel, W; Tiwari-Heckler, S, 2018) |
| "non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease in developed countries." | 1.48 | Role of the PNPLA3 polymorphism rs738409 on silymarin + vitamin E response in subjects with non-alcoholic fatty liver disease. ( Aller, R; de Luis, D; Durà, M; García Sánchez, C; Izaola, O; Laserna, C; Mora, N; Pina, M; Primo, D; Rojo, MÁ; Sigüenza, R, 2018) |
| "Nonalcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome and its prevalence increases continuously." | 1.48 | Establishment and characterization of an iPSC line from a 35 years old high grade patient with nonalcoholic fatty liver disease (30-40% steatosis) with homozygous wildtype PNPLA3 genotype. ( Adjaye, J; Bohndorf, M; Graffmann, N; Kashofer, K; Kawala, MA; Ncube, A; Wruck, W; Zatloukal, K, 2018) |
| "Nonalcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome and its prevalence increases continuously." | 1.48 | Establishment and characterization of an iPSC line from a 58 years old high grade patient with nonalcoholic fatty liver disease (70% steatosis) with homozygous wildtype PNPLA3 genotype. ( Adjaye, J; Bohndorf, M; Graffmann, N; Kashofer, K; Ncube, A; Wruck, W; Zatloukal, K, 2018) |
| "To find association of pediatric NAFLD with metabolic risk factors, and Patatin-like phospholipase domain-containing protein 3 (PNPLA3) gene polymorphism." | 1.48 | Study of Family Clustering and PNPLA3 Gene Polymorphism in Pediatric Non Alcoholic Fatty Liver Disease. ( Alam, S; Khanna, R; Rawat, D; Sarin, SK; Sharma, S; Sood, V, 2018) |
| "Non-alcoholic fatty liver disease (NAFLD) has a prevalence of approximately 30% in western countries, and is emerging as the first cause of liver cirrhosis and hepatocellular carcinoma (HCC)." | 1.48 | Promoting genetics in non-alcoholic fatty liver disease: Combined risk score through polymorphisms and clinical variables. ( Antonelli-Incalzi, R; Dell'Unto, C; Gallo, P; Picardi, A; Vespasiani-Gentilucci, U; Volpentesta, M, 2018) |
| "60 patients with NAFLD on the background of hypertension and overweight were examined." | 1.48 | [ANTHROPOMETRIC CHARACTERISTICS AND PARAMETERS OF LIPID-CARBOHYDRATE METABOLISM IN PATIENTS WITH NONALCOHOLIC FATTY LIVER DISEASE AND HYPERTENSION DEPENDING ON THE DEGREE OF HEPATIC STEATOSIS]. ( Babak, О; Bashkirova, А, 2018) |
| "Out of 778 who initially did not have NAFLD and were not heavy drinkers throughout follow-up, 338 (43." | 1.46 | Incidence and risk factors for non-alcoholic fatty liver disease: A 7-year follow-up study among urban, adult Sri Lankans. ( Dassanayaka, AS; De Silva, AP; de Silva, HJ; De Silva, ST; Kasturiratna, A; Kato, N; Kodisinghe, K; Niriella, MA; Pathmeswaran, A; Perera, R; Piyaratna, C; Rishikesawan, V; Subasinghe, CE; Takeuchi, F; Wickramasinghe, R, 2017) |
| "In the whole NAFLD cohort, 12." | 1.46 | Low Birthweight Increases the Likelihood of Severe Steatosis in Pediatric Non-Alcoholic Fatty Liver Disease. ( Alisi, A; Bizzarri, C; Bugianesi, E; Cappa, M; Dotta, A; Giannone, G; Mosca, A; Nobili, V; Panera, N; Raponi, M; Rosso, C; Veraldi, S, 2017) |
| "Non-alcoholic fatty liver disease (NAFLD) is a disorder characterized by excessive fat deposits in hepatocytes without excessive alcohol intake." | 1.46 | Identification of deleterious rare variants in MTTP, PNPLA3, and TM6SF2 in Japanese males and association studies with NAFLD. ( Boonvisut, S; Iwamoto, S; Miyashita, H; Nakayama, K; Watanabe, K; Yoshida, K, 2017) |
| "The GG genotype had 20." | 1.46 | Association of single nucleotide polymorphism at PNPLA3 with fatty liver, steatohepatitis, and cirrhosis of liver. ( Ahmad, N; Alam, S; Islam, MS; Islam, S; Mustafa, G; Saleh, AA, 2017) |
| "Liver biopsies were obtained from 54 NAFLD patients." | 1.46 | PNPLA3 variant and portal/periportal histological pattern in patients with biopsy-proven non-alcoholic fatty liver disease: a possible role for oxidative stress. ( Angelico, F; Arca, M; Baratta, F; Carnevale, R; Carpino, G; Del Ben, M; Di Costanzo, A; Gaudio, E; Labbadia, G; Overi, D; Pannitteri, G; Pastori, D; Polimeni, L; Violi, F, 2017) |
| "We recruited 515 patients with NAFLD (age 16-88 years, 280 female patients)." | 1.46 | Combined effects of the PNPLA3 rs738409, TM6SF2 rs58542926, and MBOAT7 rs641738 variants on NAFLD severity: a multicenter biopsy-based study. ( Bantel, H; Boettler, T; Demir, M; Geier, A; Kluwe, J; Krawczyk, M; Lammert, F; Pathil, A; Rau, M; Schattenberg, JM, 2017) |
| "One-hundred seventy-four NAFLD patients, who underwent liver biopsy for diagnostic work-up, were studied." | 1.46 | Low hepatic copper content and PNPLA3 polymorphism in non-alcoholic fatty liver disease in patients without metabolic syndrome. ( Aigner, E; Datz, C; Ferenci, P; Huber-Schönauer, U; Kienbacher, C; Stadlmayr, A; Stättermayer, AF; Steindl-Munda, P; Trauner, M; Traussnigg, S; Wrba, F, 2017) |
| "Non-alcoholic fatty liver disease (NAFLD) is frequently associated with atherosclerosis." | 1.46 | Non-alcoholic fatty liver disease and subclinical atherosclerosis: A comparison of metabolically- versus genetically-driven excess fat hepatic storage. ( Angelico, F; Angeloni, A; Arca, M; Baratta, F; Catalano, C; Ceci, F; Coletta, P; D'Erasmo, L; De Masi, B; Del Ben, M; Di Costanzo, A; Di Martino, M; Girelli, G; Loffredo, L; Maranghi, M; Montali, A; Perri, L; Polimeni, L, 2017) |
| "Non-alcoholic fatty liver disease (NAFLD) is becoming the most prevalent liver disorder." | 1.43 | The common PNPLA3 variant p.I148M is associated with liver fat contents as quantified by controlled attenuation parameter (CAP). ( Arslanow, A; Grünhage, F; Krawczyk, M; Lammert, F; Stokes, CS; Weber, SN, 2016) |
| "A genetic basis for NAFLD has been suggested, but only few causal genes have been identified." | 1.43 | Association study of PNPLA2 gene with histological parameters of NAFLD in an obese population. ( Aerts, E; Beckers, S; Francque, S; Hubens, G; Michielsen, P; Ruppert, M; Van Camp, JK; Van Gaal, LF; Van Hul, W; Verrijken, A; Zegers, D, 2016) |
| "In 1,447 subjects with and without NAFLD, the 148M-434E (P < 0." | 1.43 | The rs2294918 E434K variant modulates patatin-like phospholipase domain-containing 3 expression and liver damage. ( Alisi, A; Badiali, S; Craxì, A; del Menico, B; Donati, B; Dongiovanni, P; Fargion, S; Fracanzani, AL; Mancina, RM; Meroni, M; Motta, BM; Nobili, V; Petta, S; Pietrelli, A; Pingitore, P; Rametta, R; Romeo, S; Valenti, L; Xing, C, 2016) |
| "In Japanese patients with biopsy-proven NAFLD, PNPLA3 genotypes may partly affect histological features, including stage of fibrosis, but the TM6SF2 genotype does not affect histological features." | 1.43 | Relationships between Genetic Variations of PNPLA3, TM6SF2 and Histological Features of Nonalcoholic Fatty Liver Disease in Japan. ( Akuta, N; Arase, Y; Hosaka, T; Ikeda, K; Kawamura, Y; Kobayashi, M; Kumada, H; Saitoh, S; Sezaki, H; Suzuki, F; Suzuki, Y, 2016) |
| "Nonalcoholic fatty liver disease (NAFLD) is a disease caused by the accumulation of lipids in hepatocytes." | 1.43 | Depletion of Rab32 decreases intracellular lipid accumulation and induces lipolysis through enhancing ATGL expression in hepatocytes. ( Chen, D; Li, Q; Wan, Y; Wang, J, 2016) |
| "The association between nonalcoholic fatty liver disease (NAFLD) and apolipoprotein C3 gene (APOC3) promoter region single-nucleotide polymorphisms (SNPs) rs2854117 and rs2854116 is controversial." | 1.43 | APOC3 rs2070666 Is Associated with the Hepatic Steatosis Independently of PNPLA3 rs738409 in Chinese Han Patients with Nonalcoholic Fatty Liver Diseases. ( Chen, GY; Fan, JG; Mi, YQ; Pan, Q; Shen, F; Zhang, RN; Zheng, RD; Zhou, D; Zhu, CY, 2016) |
| "Since not all NAFLD with fibrosis evolve to cirrhosis, we investigated the specific risk of cirrhosis conferred in NAFLD patients by carrying this SNP." | 1.43 | The PNPLA3 rs738409 C > G polymorphism is associated with the risk of progression to cirrhosis in NAFLD patients. ( Carotti, S; De Vincentis, A; Dell'Unto, C; Galati, G; Gallo, P; Morini, S; Picardi, A; Piccioni, L; Porcari, A; Riva, E; Vespasiani-Gentilucci, U; Vorini, F, 2016) |
| "Non-alcoholic fatty liver disease (NAFLD) is considered the most common manifestation of metabolic syndrome." | 1.43 | Effects of the new thiazolidine derivative LPSF/GQ-02 on hepatic lipid metabolism pathways in non-alcoholic fatty liver disease (NAFLD). ( Araújo, S; Gomes, F; Lima, I; Lima, MDC; Oliveira, A; Oliveira, W; Peixoto, C; Pitta, I; Ribeiro, E; Soares E Silva, A, 2016) |
| "Blood samples were collected from 296 NAFLD patients and 321 healthy controls, and the genotypes of these patients were determined by PCR and genotyping." | 1.43 | [Influence of leptin receptor gene K109R polymorphism on the risk of nonalcoholic fatty liver disease and its interaction with PNPLA3 I148M polymorphism]. ( An, BQ; Cheng, YT; Jiang, M; Lu, LL; Xin, YN; Xuan, SY; Yuan, C, 2016) |
| "Obesity is the major trigger of nonalcoholic fatty liver disease (NAFLD)." | 1.43 | PNPLA3 p.I148M variant is associated with greater reduction of liver fat content after bariatric surgery. ( Alustiza, JM; Banales, JM; Bujanda, L; Emparanza, JI; Jiménez-Agüero, R; Krawczyk, M; Lammert, F; Perugorria, MJ, 2016) |
| "The mechanisms of genetic predisposition towards the development of NASH and related fibrosis remain unclear." | 1.43 | The role of mitochondrial genomics in patients with non-alcoholic steatohepatitis (NASH). ( Baranova, A; Goodman, Z; Jeiran, K; Koenig, AB; Mehta, R; Otgonsuren, M; Younossi, Z, 2016) |
| "Nonalcoholic fatty liver disease (NAFLD), the most common form of chronic liver disease, manifests as an over-accumulation of hepatic fat." | 1.43 | LncRNA SRA promotes hepatic steatosis through repressing the expression of adipose triglyceride lipase (ATGL). ( Chen, G; Koenig, RJ; Liu, J; Nian, X; Sheng, L; Xu, B; Yu, D, 2016) |
| "Significant interactions on childhood NAFLD were found between the G-allele number in the PNPLA3 rs738409 polymorphism and behaviors, including physical activity (P = 0." | 1.43 | Physical activity and sedentary behavior can modulate the effect of the PNPLA3 variant on childhood NAFLD: a case-control study in a Chinese population. ( Chawla, N; Ma, J; Meng, X; Shang, X; Song, J; Wang, H; Wang, S; Yang, Y, 2016) |
| "221 dB/m, p = 0." | 1.42 | Noninvasive characterization of graft steatosis after liver transplantation. ( Bartels, M; Berg, T; Böhm, S; Karlas, T; Keim, V; Kollmeier, J; Kovacs, P; Mössner, J; Müller, J; Rosendahl, J; Tröltzsch, M; Weimann, A; Wiegand, J, 2015) |
| "Comparison of the three NAFLD groups with similar LFATs showed that both the 'TM6SF2 NAFLD' and 'PNPLA3 NAFLD' had significantly lower triglyceride levels and were characterized by lower levels of most common TAGs compared to the 'Non-risk NAFLD' group." | 1.42 | Circulating triacylglycerol signatures and insulin sensitivity in NAFLD associated with the E167K variant in TM6SF2. ( Hyötyläinen, T; Llauradó, G; Orešič, M; Orho-Melander, M; Yki-Järvinen, H; Zhou, Y, 2015) |
| "Histological features of steatohepatitis in CHC were assessed using the Bedossa classification." | 1.42 | PNPLA3 rs738409 I748M is associated with steatohepatitis in 434 non-obese subjects with hepatitis C. ( Abate, ML; Bugianesi, E; Cabibi, D; Cammà, C; Craxì, A; Di Marco, V; Eslam, M; George, J; Grimaudo, S; Macaluso, FS; McLeod, D; Petta, S; Pipitone, RM; Rosso, C; Smedile, A; Vanni, E, 2015) |
| "Obesity is associated with non-alcoholic fatty liver disease (NAFLD), and the patatin-like phospholipase 3 (PNPLA3) rs738409 (Ile148Met, C>G) gene polymorphism is one of the most important genetic determinants of NAFLD." | 1.42 | Patatin-like phospholipase 3 (rs738409) gene polymorphism is associated with increased liver enzymes in obese adolescents and metabolic syndrome in all ages. ( Aigner, E; Baumgartner, BG; Haybaeck, J; Lackner, C; Mangge, H; Prüller, F; Reininghaus, EZ; Schnedl, WJ; Stauber, R; Weghuber, D; Zelzer, S, 2015) |
| " These negative associations between clinical risk factors and rs738409-G dosage were more prominent in non-NAFLD group compared to those in NAFLD group." | 1.42 | I148M variant in PNPLA3 reduces central adiposity and metabolic disease risks while increasing nonalcoholic fatty liver disease. ( Cho, B; Choi, HC; Hwang, KB; Kim, JI; Kong, SW; Kwon, H; Lee, IH; Park, JH; Prilutsky, D; Yun, JM, 2015) |
| "In patients with both CHB and NAFLD, these genotypes of PNPLA3 polymorphisms were associated with increased susceptibility to nonalcoholic steatohepatitis (NASH) (NAFLD activity score ≥ 3; P = 0." | 1.42 | Linked PNPLA3 polymorphisms confer susceptibility to nonalcoholic steatohepatitis and decreased viral load in chronic hepatitis B. ( Chen, GY; Chen, YM; Fan, JG; Liu, WB; Lu, JF; Mi, YQ; Pan, Q; Shen, F; Sun, WL; Wang, YQ; Zhang, RN; Zhang, SY; Zheng, RD; Zhu, CY, 2015) |
| "De novo NAFLD was more frequent in PNPLA3 GG carriers (0." | 1.42 | PNPLA3 I148M variant affects non-alcoholic fatty liver disease in liver transplant recipients. ( Chen, TC; Cheng, J; Liu, ZT; Lu, XX; Xie, HY; Zheng, SS; Zhou, L, 2015) |
| "NAFLD was defined as intrahepatic triglyceride content at ≥5% by proton-magnetic resonance spectroscopy." | 1.42 | Diet-Quality Scores and Prevalence of Nonalcoholic Fatty Liver Disease: A Population Study Using Proton-Magnetic Resonance Spectroscopy. ( Chan, FK; Chan, HL; Chan, R; Chim, AM; Chu, WC; Leung, J; Li, LS; Sea, MM; Wong, GL; Wong, VW; Woo, J; Yeung, DK, 2015) |
| "Non-alcoholic fatty liver disease (NAFLD) in non-obese individuals is inadequately elucidated." | 1.42 | The Impact of PNPLA3 rs738409 Genetic Polymorphism and Weight Gain ≥10 kg after Age 20 on Non-Alcoholic Fatty Liver Disease in Non-Obese Japanese Individuals. ( Itoh, Y; Kadotani, H; Kamaguchi, M; Kobayashi, M; Mochizuki, N; Nishimura, T; Nishioji, K; Sumida, Y; Yamaguchi, K, 2015) |
| "Non-alcoholic fatty liver disease (NAFLD) is a consequence of sedentary life style and high fat diets with an estimated prevalence of about 30% in western countries." | 1.42 | Multi-omic profiles of human non-alcoholic fatty liver disease tissue highlight heterogenic phenotypes. ( Adjaye, J; Berg, D; Daskalaki, A; Drews, K; Gralka, E; Jozefczuk, J; Kashofer, K; Korf, U; Lehrach, H; Pandey, V; Regenbrecht, C; Rehman, S; Turano, P; Westerhoff, HV; Wierling, C; Wruck, W; Zatloukal, K, 2015) |
| "Nonalcoholic fatty liver disease (NAFLD) has become the most common cause of chronic liver disease in industrialized countries in adults and children, following the trail of the epidemic diffusion of obesity." | 1.40 | A 4-polymorphism risk score predicts steatohepatitis in children with nonalcoholic fatty liver disease. ( Alisi, A; Dallapiccola, B; Donati, B; Nobili, V; Panera, N; Valenti, L; Vongsakulyanon, A, 2014) |
| "The prevalence of GG genotype in NAFLD subjects was 20." | 1.40 | PNPLA3 gene polymorphism accounts for fatty liver in community subjects without metabolic syndrome. ( Chan, AW; Chan, HL; Chan, HY; Chan, RS; Chim, AM; Choi, PC; Chu, WC; Shen, J; Wong, GL; Wong, VW; Woo, J; Yeung, DK, 2014) |
| "Non-alcoholic fatty liver disease (NAFLD) is one of the most prevalent liver diseases around the world, and is closely associated with obesity, diabetes, and insulin resistance." | 1.40 | Therapeutic role of ursolic acid on ameliorating hepatic steatosis and improving metabolic disorders in high-fat diet-induced non-alcoholic fatty liver disease rats. ( Guo, F; Li, S; Li, X; Li, Y; Liao, X; Meng, F; Meng, M; Sun, C; Sun, Z; Wang, Y, 2014) |
| "In 366 consecutive NAFLD patients (197 from Sicily, and 169 from center/northern Italy), we assessed anthropometric, biochemical and metabolic features; liver biopsy was scored according to Kleiner." | 1.40 | Glucokinase regulatory protein gene polymorphism affects liver fibrosis in non-alcoholic fatty liver disease. ( Boccia, S; Bugianesi, E; Cabibi, D; Cammà, C; Craxì, A; Di Marco, V; Grieco, A; Grimaudo, S; Marchesini, G; Miele, L; Petta, S; Pipitone, RM; Rosso, C, 2014) |
| "Although most hepatocellular carcinoma (HCC) is related to chronic viral hepatitis or alcoholic liver disease, the incidence of NAFLD-related HCC is increasing." | 1.40 | Carriage of the PNPLA3 rs738409 C >G polymorphism confers an increased risk of non-alcoholic fatty liver disease associated hepatocellular carcinoma. ( Anstee, QM; Burt, AD; Daly, AK; Day, CP; Dufour, JF; Leathart, JB; Liu, YL; Patman, GL; Piguet, AC; Reeves, HL, 2014) |
| "CT-defined fatty liver is common among men at risk for HIV infection and is associated with greater visceral adiposity, HOMA-IR, and PNPLA3 (rs738409)." | 1.40 | Risk factors for fatty liver in the Multicenter AIDS Cohort Study. ( Budoff, MJ; Kingsley, LA; Latanich, R; Palella, FJ; Post, WS; Price, JC; Seaberg, EC; Thio, CL; Witt, MD, 2014) |
| "Metabolic syndrome was defined according to ATPIII modified criteria." | 1.40 | Non-alcoholic fatty liver disease, metabolic syndrome and patatin-like phospholipase domain-containing protein3 gene variants. ( Angelico, F; Arca, M; Baratta, F; Brancorsini, M; D'Erasmo, L; Del Ben, M; Di Costanzo, A; Loffredo, L; Pastori, D; Pignatelli, P; Polimeni, L; Violi, F, 2014) |
| "A total of 339 Korean adults (155 NAFLD patients and 184 healthy controls) were enrolled." | 1.40 | Role of the PNPLA3 I148M polymorphism in nonalcoholic fatty liver disease and fibrosis in Korea. ( Byoun, YS; Jang, ES; Jeong, SH; Kim, HY; Kim, JW; Lee, SS; Woo, BH, 2014) |
| "The association of variants with NAFLD in the Uygur and Han was assessed using the chi-squared (χ2) test in different gene models." | 1.40 | Association between the PNPLA3 I148M polymorphism and non-alcoholic fatty liver disease in the Uygur and Han ethnic groups of northwestern China. ( Cai, W; Miao, L; Song, J; Xu, Q; Yao, H; Zhang, B; Zhang, L; Zhang, Y, 2014) |
| "Subjects made up of 144 biopsy-proven NAFLD patients and 198 controls were genotyped using TaqMan assays." | 1.39 | Susceptibility and gene interaction study of the angiotensin II type 1 receptor (AGTR1) gene polymorphisms with non-alcoholic fatty liver disease in a multi-ethnic population. ( Basu, RC; Cheah, PL; Mahadeva, S; Mohamed, R; Mohamed, Z; Rampal, S; Salim, A; Zain, SM, 2013) |
| "If NAFLD was suspected, liver biopsy was proposed." | 1.39 | A gene variant of PNPLA3, but not of APOC3, is associated with histological parameters of NAFLD in an obese population. ( Beckers, S; Caron, S; Francque, S; Hilden, H; Hubens, G; Michielsen, P; Ruppert, M; Staels, B; Taskinen, MR; Van Gaal, L; Van Hul, W; Van Marck, E; Verrijken, A; Zegers, D, 2013) |
| "To evaluate if the presence of carotid atherosclerosis in patients with NAFLD, could be related to gene variants influencing hepatic fat accumulation and the severity of liver damage." | 1.39 | PNPLA3 GG genotype and carotid atherosclerosis in patients with non-alcoholic fatty liver disease. ( Barcellona, MR; Cabibi, D; Cammà, C; Craxì, A; Di Marco, V; Donati, B; Fargion, S; Fracanzani, A; Grimaudo, S; Licata, A; Licata, G; Marchesini, G; Parrinello, G; Petta, S; Pipitone, RM; Torres, D; Valenti, L, 2013) |
| "The relationship of SNPs and NAFLD-related markers of liver function were assessed by correlation analysis." | 1.39 | [Polymorphism rs738409 in PNPLA3 is associated with inherited susceptibility to non-alcoholic fatty liver disease]. ( Dong, QJ; Jiang, XJ; Lin, ZH; Lü, WH; Xin, YN; Xu, J; Xuan, SY; Zhang, DD; Zhang, M, 2013) |
| "1." | 1.39 | PNPLA3 I148M polymorphism, clinical presentation, and survival in patients with hepatocellular carcinoma. ( Bertelli, C; Carnelutti, A; Colombo, M; Donati, B; Dongiovanni, P; Facchetti, F; Fargion, S; Fracanzani, AL; Iavarone, M; Motta, BM; Rametta, R; Sangiovanni, A; Soardo, G; Valenti, L, 2013) |
| "Hepatic cirrhosis was associated with a higher aspartate aminotransferase/platelet ratio index (APRI), no fatty change of the liver, higher BMI and higher AFP levels." | 1.39 | No correlation between PNPLA3 rs738409 genotype and fatty liver and hepatic cirrhosis in Japanese patients with HCV. ( Jiang, X; Kanda, T; Miyamura, T; Nakamoto, S; Nakamura, M; Wu, S; Yokosuka, O, 2013) |
| "Non-alcoholic fatty liver disease (NAFLD) is an emerging epidemic disease." | 1.39 | PNPLA3, a genetic marker of progressive liver disease, still hiding its metabolic function? ( Burnol, AF; Dubuquoy, C; Moldes, M, 2013) |
| "PNPLA3 NAFLD is characterised by an increase in liver fat but no insulin resistance or AT inflammation, while obese NAFLD has all three of these features." | 1.39 | Adipose tissue is inflamed in NAFLD due to obesity but not in NAFLD due to genetic variation in PNPLA3. ( Hakkarainen, A; Lallukka, S; Lundbom, N; Olkkonen, VM; Orho-Melander, M; Perttilä, J; Sevastianova, K; Yki-Järvinen, H, 2013) |
| "Non-alcoholic fatty liver disease (NAFLD) is a complex disease trait where genetic variations and environment interact to determine disease progression." | 1.38 | The SOD2 C47T polymorphism influences NAFLD fibrosis severity: evidence from case-control and intra-familial allele association studies. ( Al-Serri, A; Anstee, QM; Daly, AK; Day, CP; Dongiovanni, P; Fargion, S; Fracanzani, A; Leathart, JB; Nobili, V; Patch, J; Valenti, L, 2012) |
| "We developed a novel NAFLD Liver Inflammation Score, including serum Il-1RA concentration, which performed better to diagnose NASH than did previously published scores." | 1.38 | Serum interleukin 1 receptor antagonist as an independent marker of non-alcoholic steatohepatitis in humans. ( Grönlund, S; Gylling, H; Kainulainen, S; Käkelä, P; Kaminska, D; Kärjä, V; Kuulasmaa, T; Kuusisto, J; Laakso, M; Pääkkönen, M; Pihlajamäki, J; Punnonen, K; Simonen, M, 2012) |
| "A total of 144 biopsy-proven NAFLD patients and 198 controls were genotyped for PNPLA3 gene polymorphism (rs738409 C>G)." | 1.38 | A multi-ethnic study of a PNPLA3 gene variant and its association with disease severity in non-alcoholic fatty liver disease. ( Basu, RC; Cheah, PL; Mahadeva, S; Mohamed, R; Mohamed, Z; Rampal, S; Zain, SM, 2012) |
| "Nonalcoholic fatty liver disease (NAFLD) is characterized by triglyceride (TG) accumulation and endoplasmic reticulum (ER) stress." | 1.38 | Absence of adipose triglyceride lipase protects from hepatic endoplasmic reticulum stress in mice. ( Claudel, T; Fuchs, CD; Gumhold, J; Haemmerle, G; Halilbasic, E; Koefeler, H; Kumari, P; Pollheimer, MJ; Scharnagl, H; Silbert, D; Stojakovic, T; Trauner, M, 2012) |
| "One hundred sixty consecutive NAFLD patients were assessed by liver biopsy (Kleiner score); anthropometric, and biochemical and metabolic features were included." | 1.38 | IL28B and PNPLA3 polymorphisms affect histological liver damage in patients with non-alcoholic fatty liver disease. ( Cabibi, D; Cammà, C; Craxì, A; Di Marco, V; Grimaudo, S; Licata, G; Petta, S; Pipitone, RM, 2012) |
| "Non-alcoholic fatty liver disease (NAFLD) is characterized by insulin resistance." | 1.38 | Hepatic lipase activity is increased in non-alcoholic fatty liver disease beyond insulin resistance. ( Berg, G; Cacciagiú, L; Fassio, E; Gonzalez Ballerga, E; Lopez, G; Lucero, D; Miksztowicz, V; Schreier, L; Sordá, J; Zago, V, 2012) |
| "Similarly, treatment of the fatty liver cell model with alpha-lipoic acid reduced intracellular lipid accumulation in HepG2 cells, increased AMPK phosphorylation, and induced ATGL expression." | 1.38 | Alpha-lipoic acid induces adipose triglyceride lipase expression and decreases intracellular lipid accumulation in HepG2 cells. ( Chen, WL; Kuo, YT; Lee, HM; Lin, TH, 2012) |
| "Nonalcoholic fatty liver disease (NAFLD) is an escalating medical problem worldwide." | 1.38 | Genetic variant I148M in PNPLA3 is associated with the ultrasonography-determined steatosis degree in a Chinese population. ( Ku, HC; Li, Y; Tian, Z; Xing, C, 2012) |
| "The effect of the G allele on pediatric NAFLD followed a dominant genetic model." | 1.37 | A common variant in the PNPLA3 gene is a risk factor for non-alcoholic fatty liver disease in obese Taiwanese children. ( Chang, MH; Chang, PF; Hu, FC; Lin, YC; Ni, YH; Yang, WS, 2011) |
| "Non-alcoholic fatty liver disease (NAFLD) is a highly prevalent condition, particularly among Hispanic Americans." | 1.37 | Association of PNPLA3 with non-alcoholic fatty liver disease in a minority cohort: the Insulin Resistance Atherosclerosis Family Study. ( Bowden, DW; Chen, YD; Haffner, S; Langefeld, CD; Norris, JM; Palmer, ND; Rotter, JI; Scherzinger, A; Wagenknecht, LE; Ziegler, J, 2011) |
| "Non-alcoholic fatty liver disease (NAFLD) is commonly diagnosed in patients with obesity and type 2 diabetes mellitus (T2DM), and has been associated with the single nucleotide polymorphism (SNP) rs738409 in the PNPLA3 gene." | 1.37 | Association of PNPLA3 SNP rs738409 with liver density in African Americans with type 2 diabetes mellitus. ( Bowden, DW; Carr, JJ; Cox, AJ; Freedman, BI; Hightower, RC; Smith, SC; Wagenknecht, LE; Wing, MR; Xu, J, 2011) |
| "Nonalcoholic fatty liver disease (NAFLD) has recently been considered a hepatic component of insulin resistance and a risk factor in the emergence of type 2 diabetes." | 1.37 | The PNPLA3 I148M polymorphism is associated with insulin resistance and nonalcoholic fatty liver disease in a normoglycaemic population. ( Chen, SC; Chuang, WL; Dai, CY; Huang, JF; Li, SS; Lin, HY; Lin, ZY; Shin, SJ; Wang, CW; Yu, ML, 2011) |
| "Advanced liver fibrosis (stage F2 or above) was observed in 10." | 1.37 | PNPLA3 polymorphism influences liver fibrosis in unselected patients with type 2 diabetes. ( Bouillet, B; Brindisi, MC; Buffier, P; Cercueil, JP; Duvillard, L; Gambert, P; Guiu, B; Hillon, P; Jooste, V; Masson, D; Petit, JM; Robin, I; Verges, B, 2011) |
| "APOC3 SNPs were not associated with NAFLD in Italian subjects, although a borderline significance for the transmission of the -455T allele was observed in the family study." | 1.37 | The APOC3 T-455C and C-482T promoter region polymorphisms are not associated with the severity of liver damage independently of PNPLA3 I148M genotype in patients with nonalcoholic fatty liver. ( Al-Serri, A; Alterio, A; Daly, AK; Day, CP; Dongiovanni, P; Fargion, S; Fracanzani, AL; Leathart, JB; Nobili, V; Rametta, R; Roviaro, G; Valenti, L; Zappa, MA, 2011) |
| "All patients with NAFLD underwent liver biopsy." | 1.36 | Association of the rs738409 polymorphism in PNPLA3 with liver damage and the development of nonalcoholic fatty liver disease. ( Chayama, K; Hotta, K; Hyogo, H; Mizusawa, S; Nakajima, A; Nakao, K; Ochi, H; Sekine, A; Ueno, T; Yoneda, M, 2010) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 0 (0.00) | 29.6817 |
| 2010's | 250 (66.14) | 24.3611 |
| 2020's | 128 (33.86) | 2.80 |
| Authors | Studies |
|---|---|
| Franco, S | 1 |
| Horneros, J | 1 |
| Soldevila, L | 1 |
| Ouchi, D | 1 |
| Galván-Femenía, I | 1 |
| de Cid, R | 1 |
| Tenesa, M | 1 |
| Bechini, J | 1 |
| Perez, R | 1 |
| Llibre, JM | 1 |
| Clotet, B | 1 |
| Tural, C | 1 |
| Martínez, MA | 1 |
| Lee, KJ | 1 |
| Moon, JS | 1 |
| Kim, NY | 1 |
| Ko, JS | 1 |
| Kamada, Y | 1 |
| Takahashi, H | 1 |
| Shimizu, M | 1 |
| Kawaguchi, T | 1 |
| Sumida, Y | 2 |
| Fujii, H | 1 |
| Seko, Y | 5 |
| Fukunishi, S | 1 |
| Tokushige, K | 3 |
| Nakajima, A | 7 |
| Okanoue, T | 4 |
| Roe, JD | 1 |
| Garcia, LA | 1 |
| Klimentidis, YC | 2 |
| Coletta, DK | 1 |
| Shao, X | 1 |
| Uojima, H | 1 |
| Arai, T | 2 |
| Ogawa, Y | 4 |
| Setsu, T | 1 |
| Atsukawa, M | 2 |
| Furuichi, Y | 1 |
| Arase, Y | 3 |
| Horio, K | 1 |
| Hidaka, H | 1 |
| Nakazawa, T | 1 |
| Kako, M | 1 |
| Kagawa, T | 1 |
| Iwakiri, K | 2 |
| Terai, S | 1 |
| Tanaka, Y | 3 |
| Koizumi, W | 1 |
| Gavril, OI | 1 |
| Arhire, LI | 1 |
| Gavril, RS | 1 |
| Zota, MI | 1 |
| Gherasim, A | 1 |
| Nita, O | 1 |
| Drugescu, A | 1 |
| Oprescu, AC | 1 |
| Esanu, IM | 1 |
| Mitu, F | 1 |
| Graur, M | 1 |
| Mihalache, L | 1 |
| Liu, WY | 4 |
| Zhang, X | 3 |
| Li, G | 3 |
| Tang, LJ | 2 |
| Zhu, PW | 6 |
| Rios, RS | 2 |
| Zheng, KI | 6 |
| Ma, HL | 5 |
| Wang, XD | 7 |
| Pan, Q | 4 |
| de Knegt, RJ | 1 |
| Valenti, L | 21 |
| Ghanbari, M | 1 |
| Zheng, MH | 7 |
| Rady, B | 1 |
| Nishio, T | 1 |
| Dhar, D | 2 |
| Liu, X | 2 |
| Erion, M | 1 |
| Kisseleva, T | 1 |
| Brenner, DA | 1 |
| Pocai, A | 1 |
| Cherubini, A | 2 |
| Casirati, E | 1 |
| Tomasi, M | 1 |
| Liu, Z | 5 |
| Chen, X | 2 |
| Xia, M | 1 |
| Ma, S | 1 |
| Huang, Q | 1 |
| Zeng, H | 1 |
| Ge, J | 1 |
| Xu, W | 1 |
| Wu, Q | 1 |
| Wu, L | 3 |
| Li, X | 7 |
| Ma, H | 4 |
| Chen, L | 2 |
| Li, Q | 4 |
| Aleteng, Q | 3 |
| Hu, Y | 3 |
| He, W | 1 |
| Pan, B | 1 |
| Lin, H | 1 |
| Zheng, Y | 1 |
| Wang, S | 3 |
| Tang, H | 1 |
| Gao, X | 4 |
| Pirola, CJ | 8 |
| Salatino, A | 1 |
| Quintanilla, MF | 1 |
| Castaño, GO | 1 |
| Garaycoechea, M | 1 |
| Sookoian, S | 8 |
| Di Sessa, A | 7 |
| Russo, MC | 1 |
| Arienzo, MR | 1 |
| Umano, GR | 6 |
| Cozzolino, D | 3 |
| Cirillo, G | 8 |
| Guarino, S | 5 |
| Miraglia Del Giudice, E | 8 |
| Marzuillo, P | 7 |
| Schmidt, KA | 1 |
| Jones, RB | 1 |
| Rios, C | 1 |
| Corona, Y | 1 |
| Berger, PK | 1 |
| Plows, JF | 1 |
| Alderete, TL | 2 |
| Fogel, J | 1 |
| Hampson, H | 1 |
| Hartiala, JA | 1 |
| Cai, Z | 1 |
| Allayee, H | 2 |
| Nayak, KS | 1 |
| Sinatra, FR | 1 |
| Harlan, G | 1 |
| Pickering, TA | 1 |
| Salvy, SJ | 1 |
| Mack, WJ | 1 |
| Kohli, R | 1 |
| Goran, MI | 2 |
| Cinque, F | 1 |
| Cespiati, A | 2 |
| Lombardi, R | 4 |
| Costantino, A | 1 |
| Maffi, G | 1 |
| Alletto, F | 1 |
| Colavolpe, L | 1 |
| Francione, P | 1 |
| Oberti, G | 1 |
| Fatta, E | 1 |
| Bertelli, C | 2 |
| Sigon, G | 1 |
| Dongiovanni, P | 13 |
| Vecchi, M | 1 |
| Fargion, S | 12 |
| Fracanzani, AL | 7 |
| Yuan, F | 1 |
| Gu, Z | 1 |
| Bi, Y | 1 |
| Yuan, R | 1 |
| Niu, W | 1 |
| Ren, D | 1 |
| Zhang, L | 3 |
| He, G | 1 |
| Liu, BC | 1 |
| Vilar-Gomez, E | 2 |
| Wilson, LA | 2 |
| Liang, T | 3 |
| Chalasani, N | 5 |
| Oliveira, CP | 2 |
| Mana, MF | 1 |
| Parisi, MCR | 1 |
| Correa-Giannella, ML | 1 |
| Neto, AM | 1 |
| Yamanaka, A | 1 |
| Cunha-Silva, M | 1 |
| Cavaleiro, AM | 1 |
| Dos Santos, CR | 1 |
| Pavan, CR | 1 |
| Sevá-Pereira, T | 1 |
| Dertkigil, SSJ | 1 |
| Mazo, DF | 2 |
| Vujkovic, M | 3 |
| Ramdas, S | 1 |
| Lorenz, KM | 1 |
| Guo, X | 2 |
| Darlay, R | 2 |
| Cordell, HJ | 2 |
| He, J | 1 |
| Gindin, Y | 1 |
| Chung, C | 1 |
| Myers, RP | 1 |
| Schneider, CV | 2 |
| Park, J | 2 |
| Lee, KM | 2 |
| Serper, M | 2 |
| Carr, RM | 3 |
| Kaplan, DE | 2 |
| Haas, ME | 1 |
| MacLean, MT | 1 |
| Witschey, WR | 1 |
| Zhu, X | 1 |
| Tcheandjieu, C | 1 |
| Kember, RL | 1 |
| Kranzler, HR | 2 |
| Verma, A | 1 |
| Giri, A | 1 |
| Klarin, DM | 1 |
| Sun, YV | 1 |
| Huang, J | 1 |
| Huffman, JE | 1 |
| Creasy, KT | 1 |
| Hand, NJ | 1 |
| Liu, CT | 1 |
| Long, MT | 1 |
| Yao, J | 1 |
| Budoff, M | 1 |
| Tan, J | 1 |
| Lin, HJ | 1 |
| Chen, YI | 2 |
| Taylor, KD | 2 |
| Chang, RK | 1 |
| Krauss, RM | 2 |
| Vilarinho, S | 1 |
| Brancale, J | 1 |
| Nielsen, JB | 1 |
| Locke, AE | 1 |
| Jones, MB | 1 |
| Verweij, N | 1 |
| Baras, A | 1 |
| Reddy, KR | 1 |
| Neuschwander-Tetri, BA | 1 |
| Schwimmer, JB | 2 |
| Sanyal, AJ | 3 |
| Ryan, KA | 1 |
| Mitchell, BD | 2 |
| Gill, D | 1 |
| Wells, AD | 1 |
| Manduchi, E | 1 |
| Saiman, Y | 1 |
| Mahmud, N | 1 |
| Miller, DR | 2 |
| Reaven, PD | 2 |
| Phillips, LS | 2 |
| Muralidhar, S | 2 |
| DuVall, SL | 2 |
| Lee, JS | 2 |
| Assimes, TL | 2 |
| Pyarajan, S | 2 |
| Cho, K | 1 |
| Edwards, TL | 1 |
| Damrauer, SM | 2 |
| Wilson, PW | 1 |
| Gaziano, JM | 2 |
| O'Donnell, CJ | 3 |
| Khera, AV | 1 |
| Grant, SFA | 1 |
| Brown, CD | 1 |
| Tsao, PS | 2 |
| Saleheen, D | 2 |
| Lotta, LA | 1 |
| Bastarache, L | 1 |
| Anstee, QM | 8 |
| Daly, AK | 6 |
| Meigs, JB | 2 |
| Rotter, JI | 3 |
| Lynch, JA | 2 |
| Rader, DJ | 3 |
| Voight, BF | 3 |
| Chang, KM | 2 |
| Pan, XY | 5 |
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| Huang, OY | 1 |
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| Targher, G | 11 |
| Byrne, CD | 14 |
| Ericson, E | 1 |
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| Quiroga, AD | 1 |
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| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| Diets Based on PNPLA3 Genotype for Reducing Liver Fat in Hispanics With Pediatric Non-alcoholic Fatty Liver Disease[NCT02948647] | 113 participants (Actual) | Interventional | 2016-11-30 | Completed | |||
| Mechanisms of Obesity and Its Metabolic Complications in Youth[NCT03454828] | 100 participants (Anticipated) | Interventional | 2018-05-01 | Recruiting | |||
| Pathogenesis of the Cardiometabolic Risk in Youth With Type 1 Diabetes[NCT04101045] | 7 participants (Actual) | Interventional | 2019-11-21 | Terminated (stopped due to During the pandemic the funding agency stopped funding studies.) | |||
| Prospective Study on Diabetes Mellitus and Its Complications in Newly Diagnosed Adult Patients[NCT01055093] | 2,000 participants (Anticipated) | Observational | 2005-09-30 | Recruiting | |||
| Effect of Oral Semaglutide on Liver Fat and Body Composition in Liver Transplant Recipients With Diabetes Mellitus: Sema-Lit[NCT06060392] | 50 participants (Anticipated) | Interventional | 2023-10-30 | Recruiting | |||
| This Trial is Conducted Globally. The Aim of This Trial is to Investigate Efficacy and Safety of Three Dose Levels of Subcutaneous Semaglutide Once Daily Versus Placebo in Subjects With Non-alcoholic Steatohepatitis[NCT02970942] | Phase 2 | 320 participants (Actual) | Interventional | 2016-11-30 | Completed | ||
| The Effects of Dietary Supplementation on Hepatic Insulin Action and Glucose Tolerance in Pre-diabetes[NCT01729078] | 48 participants (Actual) | Interventional | 2012-10-31 | Completed | |||
| Non Invasive Evaluation of Liver Fibrosis and Steatosis in Type 2 Diabetic Patient in Assiut University Hospitals[NCT05605717] | 60 participants (Anticipated) | Observational | 2022-11-01 | Not yet recruiting | |||
| Clinical Study on the Value of Quantitative MRI Imaging in Diffuse Liver Diseases[NCT04626492] | 150 participants (Anticipated) | Observational [Patient Registry] | 2020-08-01 | Recruiting | |||
| Effect of Intermittent Calorie Restriction on Metabolic Dysfunction-Associated Steatotic Liver Disease Patients With Abnormal Glucose Metabolism[NCT04283942] | 60 participants (Actual) | Interventional | 2020-07-30 | Completed | |||
| Establishment of Non-alcoholic Fatty Liver Disease Cohort and Development of Markers to Predict Histologic Progression of Liver Fibrosis[NCT02206841] | 1,000 participants (Anticipated) | Observational [Patient Registry] | 2014-01-01 | Recruiting | |||
| The Role of Microbiome Reprogramming on Liver Fat Accumulation[NCT03914495] | 57 participants (Actual) | Interventional | 2019-05-21 | Terminated (stopped due to PI carefully considered multiple factors and decided to close study to any further enrollment.) | |||
| Comparative Clinical Study to Evaluate the Possible Beneficial Effect of Empagliflozin Versus Pioglitazone on Non-diabetic Patients With Non-Alcoholic Steatohepatitis[NCT05605158] | Phase 3 | 56 participants (Anticipated) | Interventional | 2022-11-30 | Not yet recruiting | ||
| Study of Efficacy and Tolerability of Docosahexaenoic Acid (DHA) on Children Affected by Nonalcoholic Fatty Liver Disease (NAFLD).[NCT00885313] | Phase 1/Phase 2 | 60 participants (Actual) | Interventional | 2009-03-31 | Completed | ||
| Prevalence, Clinicopathological Characteristics, Biomarkers and Genetics of Nonalcoholic Steatohepatitis in Taiwanese Children[NCT00274183] | 614 participants (Actual) | Observational | 2006-01-31 | Completed | |||
| Study for the Investigation of New Individual Risk Profiles and Therapeutic Strategies in Obesity Related Cardiovascular and Metabolic Disorders.[NCT00482924] | 1,500 participants (Anticipated) | Observational | 2003-01-31 | Recruiting | |||
| The Effects of Purified n-3 Fatty Acids on Serum Fibrosis Markers and Cardiovascular Risk Markers in a Randomized Placebo Controlled Trial in Patients With Non Alcoholic Fatty Liver Disease[NCT00760513] | Phase 4 | 103 participants (Actual) | Interventional | 2009-11-01 | Completed | ||
| Efficacy of Nutritional Therapy With High Methionine Content in the Treatment of Non-alcoholic Fatty Liver: a Randomized Clinical Trial[NCT04450875] | 121 participants (Actual) | Interventional | 2015-03-24 | Completed | |||
| A Gender and Culturally Specific Approach to Reduce NAFLD in Mexican-American Men[NCT04186260] | 39 participants (Anticipated) | Interventional | 2023-12-01 | Recruiting | |||
| Genetic-specific Effects of Fructose on Liver Lipogenesis[NCT03783195] | 15 participants (Actual) | Interventional | 2019-01-25 | Completed | |||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
Change in ALT (measured as units per liter) is presented as ratio to baseline. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Ratio of ALT (Geometric Mean) |
|---|---|
| Semaglutide 0.1 mg | 0.62 |
| Semaglutide 0.2 mg | 0.57 |
| Semaglutide 0.4 mg | 0.40 |
| Placebo | 0.80 |
Change in albumin (measured as grams per deciliter) is presented as ratio to baseline. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Ratio of albumin (Geometric Mean) |
|---|---|
| Semaglutide 0.1 mg | 1.02 |
| Semaglutide 0.2 mg | 1.01 |
| Semaglutide 0.4 mg | 1.01 |
| Placebo | 1.02 |
Change in alkaline phosphatase (measured as units per liter) is presented as ratio to baseline. The endpoint was evaluated based on the data from on-treatment period. On-treatment period: the period starting on the date of first administration of trial product and ending on the date of the last dose of trial product +7 days; except for the evaluation of AEs and hypoglycaemic episodes for which the period ended on the date of whatever came first: 1) last dose of trial product + 49 days (7 half-lives of semaglutide); 2) end of the in-trial period. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Ratio of alkaline phosphatase (Geometric Mean) |
|---|---|
| Semaglutide 0.1 mg | 0.980 |
| Semaglutide 0.2 mg | 0.931 |
| Semaglutide 0.4 mg | 0.884 |
| Placebo | 0.992 |
Change in amylase (measured as units per liter) is presented as ratio to baseline. The endpoint was evaluated based on the data from on-treatment period. On-treatment period: the period starting on the date of first administration of trial product and ending on the date of the last dose of trial product +7 days; except for the evaluation of AEs and hypoglycaemic episodes for which the period ended on the date of whatever came first: 1) last dose of trial product + 49 days (7 half-lives of semaglutide); 2) end of the in-trial period. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Ratio of amylase (Geometric Mean) |
|---|---|
| Semaglutide 0.1 mg | 1.155 |
| Semaglutide 0.2 mg | 1.120 |
| Semaglutide 0.4 mg | 1.170 |
| Placebo | 1.051 |
Change in AST (measured as units per liter) is presented as ratio to baseline. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Ratio of AST (Geometric Mean) |
|---|---|
| Semaglutide 0.1 mg | 0.66 |
| Semaglutide 0.2 mg | 0.63 |
| Semaglutide 0.4 mg | 0.50 |
| Placebo | 0.84 |
Change in BMI from baseline to week 72 is presented. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Kilograms per square meter (Mean) |
|---|---|
| Semaglutide 0.1 mg | -1.8 |
| Semaglutide 0.2 mg | -3.5 |
| Semaglutide 0.4 mg | -4.6 |
| Placebo | -0.3 |
Change in body weight from baseline to week 72 is presented. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Kilograms (Mean) |
|---|---|
| Semaglutide 0.1 mg | -4.8 |
| Semaglutide 0.2 mg | -9.4 |
| Semaglutide 0.4 mg | -12.3 |
| Placebo | -1.0 |
Change in calcitonin (measured as nanograms per liter) is presented as ratio to baseline. The endpoint was evaluated based on the data from on-treatment period. On-treatment period: the period starting on the date of first administration of trial product and ending on the date of the last dose of trial product +7 days; except for the evaluation of AEs and hypoglycaemic episodes for which the period ended on the date of whatever came first: 1) last dose of trial product + 49 days (7 half-lives of semaglutide); 2) end of the in-trial period. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Ratio of Calcitonin (Geometric Mean) |
|---|---|
| Semaglutide 0.1 mg | 1.040 |
| Semaglutide 0.2 mg | 0.937 |
| Semaglutide 0.4 mg | 1.000 |
| Placebo | 0.950 |
Change in calcium (measured as milligram per deciliter (mg/dL)) is presented as ratio to baseline. The endpoint was evaluated based on the data from on-treatment period. On-treatment period: the period starting on the date of first administration of trial product and ending on the date of the last dose of trial product +7 days; except for the evaluation of AEs and hypoglycaemic episodes for which the period ended on the date of whatever came first: 1) last dose of trial product + 49 days (7 half-lives of semaglutide); 2) end of the in-trial period. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Ratio of calcium (Geometric Mean) |
|---|---|
| Semaglutide 0.1 mg | 1.017 |
| Semaglutide 0.2 mg | 1.018 |
| Semaglutide 0.4 mg | 1.008 |
| Placebo | 1.010 |
Change in calcium (measured as mmol/L) is presented as ratio to baseline. The endpoint was evaluated based on the data from on-treatment period. On-treatment period: the period starting on the date of first administration of trial product and ending on the date of the last dose of trial product +7 days; except for the evaluation of AEs and hypoglycaemic episodes for which the period ended on the date of whatever came first: 1) last dose of trial product + 49 days (7 half-lives of semaglutide); 2) end of the in-trial period. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Ratio of calcium (Geometric Mean) |
|---|---|
| Semaglutide 0.1 mg | 1.017 |
| Semaglutide 0.2 mg | 1.018 |
| Semaglutide 0.4 mg | 1.008 |
| Placebo | 1.010 |
Change in creatine kinase (measured as units per liter) is presented as ratio to baseline. The endpoint was evaluated based on the data from on-treatment period. On-treatment period: the period starting on the date of first administration of trial product and ending on the date of the last dose of trial product +7 days; except for the evaluation of AEs and hypoglycaemic episodes for which the period ended on the date of whatever came first: 1) last dose of trial product + 49 days (7 half-lives of semaglutide); 2) end of the in-trial period. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Ratio of creatine kinase (Geometric Mean) |
|---|---|
| Semaglutide 0.1 mg | 0.975 |
| Semaglutide 0.2 mg | 0.798 |
| Semaglutide 0.4 mg | 0.825 |
| Placebo | 0.904 |
Change in creatinine (measured as milligram per deciliter (mg/dL)) is presented as ratio to baseline. The endpoint was evaluated based on the data from on-treatment period. On-treatment period: the period starting on the date of first administration of trial product and ending on the date of the last dose of trial product +7 days; except for the evaluation of AEs and hypoglycaemic episodes for which the period ended on the date of whatever came first: 1) last dose of trial product + 49 days (7 half-lives of semaglutide); 2) end of the in-trial period. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Ratio of creatinine (Geometric Mean) |
|---|---|
| Semaglutide 0.1 mg | 1.018 |
| Semaglutide 0.2 mg | 1.069 |
| Semaglutide 0.4 mg | 1.026 |
| Placebo | 1.021 |
Change in creatinine (measured as micro mole per liter (umol/L)) is presented as ratio to baseline. The endpoint was evaluated based on the data from on-treatment period. On-treatment period: the period starting on the date of first administration of trial product and ending on the date of the last dose of trial product +7 days; except for the evaluation of AEs and hypoglycaemic episodes for which the period ended on the date of whatever came first: 1) last dose of trial product + 49 days (7 half-lives of semaglutide); 2) end of the in-trial period. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Ratio of creatinine (Geometric Mean) |
|---|---|
| Semaglutide 0.1 mg | 1.018 |
| Semaglutide 0.2 mg | 1.069 |
| Semaglutide 0.4 mg | 1.026 |
| Placebo | 1.021 |
Blood pressure was measured in a sitting position after 5 minutes of rest. Change in DBP from baseline to week 72 is presented. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Millimeters of mercury (Mean) |
|---|---|
| Semaglutide 0.1 mg | 0 |
| Semaglutide 0.2 mg | -2 |
| Semaglutide 0.4 mg | -2 |
| Placebo | -1 |
Change in ELF from baseline to week 72 is presented. The ELF discriminant score was derived as a log-linear combination of the markers hyaluronic acid (HA), amino-terminal propeptide of type III collagen (PIIINP) and tissue inhibitor of metalloproteinase 1 (TIMP1). ELF score = -7.412 + 0.681 × ln(HA (nanograms per millilitre (ng/mL)) + 0.775 × ln(P3NP (ng/mL)) + 0.494 × ln(TIMP1 (ng/mL)). ELF score: a) < 7.7: no to mild fibrosis; b) ≥ 7.7 - < 9.8: Moderate fibrosis; c) ≥ 9.8 - < 11.3: Severe fibrosis; d) ≥ 11.3: Cirrhosis. A negative change from baseline indicates decreased fibrosis. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | score on a scale (Mean) |
|---|---|
| Semaglutide 0.1 mg | -0.4 |
| Semaglutide 0.2 mg | -0.4 |
| Semaglutide 0.4 mg | -0.6 |
| Placebo | 0.1 |
Change in erythrocytes from baseline to week 72 is presented. The endpoint was evaluated based on the data from on-treatment period. On-treatment period: the period starting on the date of first administration of trial product and ending on the date of the last dose of trial product +7 days; except for the evaluation of AEs and hypoglycaemic episodes for which the period ended on the date of whatever came first: 1) last dose of trial product + 49 days (7 half-lives of semaglutide); 2) end of the in-trial period. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | 10^12 cells per liter (10^12/L) (Mean) |
|---|---|
| Semaglutide 0.1 mg | 0.038 |
| Semaglutide 0.2 mg | 0.004 |
| Semaglutide 0.4 mg | -0.034 |
| Placebo | 0.054 |
Change in eGFR (measured as milliliter/minute/1.732 meter square (mL/min/1.73 m^2)) is presented as ratio to baseline. The endpoint was evaluated based on the data from on-treatment period. On-treatment period: the period starting on the date of first administration of trial product and ending on the date of the last dose of trial product +7 days; except for the evaluation of AEs and hypoglycaemic episodes for which the period ended on the date of whatever came first: 1) last dose of trial product + 49 days (7 half-lives of semaglutide); 2) end of the in-trial period. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Ratio of eGFR (Geometric Mean) |
|---|---|
| Semaglutide 0.1 mg | 0.976 |
| Semaglutide 0.2 mg | 0.940 |
| Semaglutide 0.4 mg | 0.973 |
| Placebo | 0.969 |
Change in fasting glucagon (measured as picograms per milliliter) is presented as ratio to baseline. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Ratio of glucagon (Geometric Mean) |
|---|---|
| Semaglutide 0.1 mg | 0.78 |
| Semaglutide 0.2 mg | 0.65 |
| Semaglutide 0.4 mg | 0.63 |
| Placebo | 1.04 |
Change in FPG from baseline to week 72 is presented. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Millimoles per liter (Mean) |
|---|---|
| Semaglutide 0.1 mg | -1.39 |
| Semaglutide 0.2 mg | -2.17 |
| Semaglutide 0.4 mg | -2.09 |
| Placebo | -0.34 |
Change in ferritin (measured as microgram per liter) is presented as ratio to baseline. The endpoint was evaluated based on the data from on-treatment period. On-treatment period: the period starting on the date of first administration of trial product and ending on the date of the last dose of trial product +7 days; except for the evaluation of AEs and hypoglycaemic episodes for which the period ended on the date of whatever came first: 1) last dose of trial product + 49 days (7 half-lives of semaglutide); 2) end of the in-trial period. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Ratio of ferritin (Geometric Mean) |
|---|---|
| Semaglutide 0.1 mg | 0.660 |
| Semaglutide 0.2 mg | 0.617 |
| Semaglutide 0.4 mg | 0.603 |
| Placebo | 0.713 |
Change in FGF-21 (measured as picograms per milliliter) is presented as ratio to baseline. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Ratio of FGF-21 (Geometric Mean) |
|---|---|
| Semaglutide 0.1 mg | 0.72 |
| Semaglutide 0.2 mg | 0.61 |
| Semaglutide 0.4 mg | 0.55 |
| Placebo | 0.76 |
Change in fibrosis-4 score is presented as ratio to baseline. Fibrosis-4 is the ratio of age in years and aminotransferase to platelet count. It is a non-invasive hepatic fibrosis index score combining standard biochemical values, platelets, alanine aminotransferase (ALT), AST and age that is calculated using formula: Fibrosis-4 = (Age [years] x AST [U/L]) / (platelets [10^9/L] x (square root of ALT [U/L])). A Fibrosis-4 index of < 1.45 indicated no or moderate fibrosis and an index of > 3.25 indicated extensive fibrosis/cirrhosis. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Ratio of fibrosis-4 score (Geometric Mean) |
|---|---|
| Semaglutide 0.1 mg | 0.81 |
| Semaglutide 0.2 mg | 0.77 |
| Semaglutide 0.4 mg | 0.77 |
| Placebo | 0.95 |
Change in free fatty acids (measured as millimoles per liter) is presented as ratio to baseline. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Ratio of free fatty acids (Geometric Mean) |
|---|---|
| Semaglutide 0.1 mg | 0.83 |
| Semaglutide 0.2 mg | 0.92 |
| Semaglutide 0.4 mg | 0.72 |
| Placebo | 1.05 |
Change in GGT (measured as units per liter) is presented as ratio to baseline. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Ratio of GGT (Geometric Mean) |
|---|---|
| Semaglutide 0.1 mg | 0.76 |
| Semaglutide 0.2 mg | 0.64 |
| Semaglutide 0.4 mg | 0.48 |
| Placebo | 0.92 |
Change in HbA1c (measured as percentage point of HbA1c) from baseline to week 72 is presented. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Percentage point of HbA1c (Mean) |
|---|---|
| Semaglutide 0.1 mg | -0.7 |
| Semaglutide 0.2 mg | -1.2 |
| Semaglutide 0.4 mg | -1.2 |
| Placebo | -0.0 |
Change in haematocrit from baseline to week 72 is presented. The endpoint was evaluated based on the data from on-treatment period. On-treatment period: the period starting on the date of first administration of trial product and ending on the date of the last dose of trial product +7 days; except for the evaluation of AEs and hypoglycaemic episodes for which the period ended on the date of whatever came first: 1) last dose of trial product + 49 days (7 half-lives of semaglutide); 2) end of the in-trial period. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Percentage of haematocrit in blood (Mean) |
|---|---|
| Semaglutide 0.1 mg | -0.79 |
| Semaglutide 0.2 mg | -0.71 |
| Semaglutide 0.4 mg | -1.43 |
| Placebo | -0.41 |
Change in haemoglobin from baseline to week 72 is presented. The endpoint was evaluated based on the data from on-treatment period. On-treatment period: the period starting on the date of first administration of trial product and ending on the date of the last dose of trial product +7 days; except for the evaluation of AEs and hypoglycaemic episodes for which the period ended on the date of whatever came first: 1) last dose of trial product + 49 days (7 half-lives of semaglutide); 2) end of the in-trial period. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Grams per deciliter (g/dL) (Mean) |
|---|---|
| Semaglutide 0.1 mg | 0.18 |
| Semaglutide 0.2 mg | 0.08 |
| Semaglutide 0.4 mg | -0.07 |
| Placebo | 0.21 |
Change in haemoglobin from baseline to week 72 is presented. The endpoint was evaluated based on the data from on-treatment period. On-treatment period: the period starting on the date of first administration of trial product and ending on the date of the last dose of trial product +7 days; except for the evaluation of AEs and hypoglycaemic episodes for which the period ended on the date of whatever came first: 1) last dose of trial product + 49 days (7 half-lives of semaglutide); 2) end of the in-trial period. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | millimoles per liter (mmol/L) (Mean) |
|---|---|
| Semaglutide 0.1 mg | 0.11 |
| Semaglutide 0.2 mg | 0.05 |
| Semaglutide 0.4 mg | -0.05 |
| Placebo | 0.13 |
Change in HbA1c from baseline to week 72 is presented. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | millimoles per mole (Mean) |
|---|---|
| Semaglutide 0.1 mg | -7.9 |
| Semaglutide 0.2 mg | -12.8 |
| Semaglutide 0.4 mg | -12.8 |
| Placebo | -0.3 |
Change in HDL cholesterol (measured as millimoles per liter) is presented as ratio to baseline. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Ratio of HDL cholesterol (Geometric Mean) |
|---|---|
| Semaglutide 0.1 mg | 1.04 |
| Semaglutide 0.2 mg | 1.05 |
| Semaglutide 0.4 mg | 1.09 |
| Placebo | 1.01 |
Change in hsCRP (measured as milligram per liter) from baseline to week 72 is presented as ratio to baseline. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Ratio of hsCRP (Geometric Mean) |
|---|---|
| Semaglutide 0.1 mg | 0.78 |
| Semaglutide 0.2 mg | 0.50 |
| Semaglutide 0.4 mg | 0.41 |
| Placebo | 0.91 |
Change in HOMA-IR is presented as ratio to baseline. HOMA-IR was calculated as: Insulin resistance (%) = fasting plasma glucose [mmol/L] x fasting insulin [mmol/L]/ 22.5. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Ratio of HOMA-IR (Geometric Mean) |
|---|---|
| Semaglutide 0.1 mg | 0.77 |
| Semaglutide 0.2 mg | 0.60 |
| Semaglutide 0.4 mg | 0.58 |
| Placebo | 0.81 |
Change in interleukin-1 receptor (IL-1R) antagonist (measured as picograms per milliliter) antagonist is presented as ratio to baseline. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Ratio of IL-1R antagonist (Geometric Mean) |
|---|---|
| Semaglutide 0.1 mg | 0.87 |
| Semaglutide 0.2 mg | 0.85 |
| Semaglutide 0.4 mg | 0.73 |
| Placebo | 0.94 |
Change in INR is presented as ratio to baseline. INR is the ratio of measured prothrombin time over normal prothrombin time and it evaluates the extrinsic coagulation pathway (vitamin K dependent clotting factors II; V, VII, IX and X). These clotting factors are synthesised in the liver, thus INR is used as a marker of liver synthesis function. The therapeutic INR range varies, most commonly an INR 2-3 goal, but ranging from 1.5-4.0. Bleeding complications are more likely to occur above an INR value of 4.0. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Ratio of INR (Geometric Mean) |
|---|---|
| Semaglutide 0.1 mg | 0.97 |
| Semaglutide 0.2 mg | 0.96 |
| Semaglutide 0.4 mg | 0.93 |
| Placebo | 0.99 |
Change in leukocytes from baseline to week 72 is presented. The endpoint was evaluated based on the data from on-treatment period. On-treatment period: the period starting on the date of first administration of trial product and ending on the date of the last dose of trial product +7 days; except for the evaluation of AEs and hypoglycaemic episodes for which the period ended on the date of whatever came first: 1) last dose of trial product + 49 days (7 half-lives of semaglutide); 2) end of the in-trial period. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | 10^9 cells per liter (10^9/L) (Mean) |
|---|---|
| Semaglutide 0.1 mg | 0.489 |
| Semaglutide 0.2 mg | 0.260 |
| Semaglutide 0.4 mg | -0.047 |
| Placebo | 0.075 |
Change in lipase (measured as units per liter) is presented as ratio to baseline. The endpoint was evaluated based on the data from on-treatment period. On-treatment period: the period starting on the date of first administration of trial product and ending on the date of the last dose of trial product +7 days; except for the evaluation of AEs and hypoglycaemic episodes for which the period ended on the date of whatever came first: 1) last dose of trial product + 49 days (7 half-lives of semaglutide); 2) end of the in-trial period. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Ratio of lipase (Geometric Mean) |
|---|---|
| Semaglutide 0.1 mg | 1.305 |
| Semaglutide 0.2 mg | 1.245 |
| Semaglutide 0.4 mg | 1.375 |
| Placebo | 1.003 |
Change in liver steatosis assessed by FibroScan® from baseline to week 72 is presented. FibroScan® is a specialized ultrasound machine for the liver. It measures fibrosis (scarring) and steatosis (fatty change) in the liver. Fatty change is fat building up in the liver cells. To assess liver steatosis, the controlled attenuation parameter (CAP; giving an estimate of ultrasound attenuation ∼3.5 MegaHertz (MHz)) is available with the M probe of the FibroScan. The CAP score is measured in decibels per meter (dB/m). It ranges from 100 to 400 dB/m, with higher scores indicating higher amount of liver with fatty change. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Decibels per meter (Mean) |
|---|---|
| Semaglutide 0.1 mg | -5.8 |
| Semaglutide 0.2 mg | -50.9 |
| Semaglutide 0.4 mg | -42.1 |
| Placebo | -18.7 |
Change in liver stiffness (measured as kilopascal (kPa)) assessed by FibroScan® is presented as ratio to baseline. FibroScan® is a specialized ultrasound machine for the liver. It measures fibrosis (scarring) by measuring the stiffness of the liver. It's normally between 2 and 6 kPa. Many people with liver disease(s) have a result that's higher than the normal range. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Ratio of liver stiffness (Geometric Mean) |
|---|---|
| Semaglutide 0.1 mg | 0.72 |
| Semaglutide 0.2 mg | 0.64 |
| Semaglutide 0.4 mg | 0.66 |
| Placebo | 1.18 |
Change in LDL cholesterol (measured as millimoles per liter) is presented as ratio to baseline. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Ratio of LDL cholesterol (Geometric Mean) |
|---|---|
| Semaglutide 0.1 mg | 0.96 |
| Semaglutide 0.2 mg | 1.01 |
| Semaglutide 0.4 mg | 0.92 |
| Placebo | 0.90 |
Change in miR-122 (measured as 1/microliter) is presented as ratio to baseline. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Ratio of miR-122 (Geometric Mean) |
|---|---|
| Semaglutide 0.1 mg | 0.86 |
| Semaglutide 0.2 mg | 0.74 |
| Semaglutide 0.4 mg | 0.58 |
| Placebo | 1.28 |
Change in MCP-1 (measured as picograms per milliliter) is presented as ratio to baseline. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Ratio of MCP-1 (Geometric Mean) |
|---|---|
| Semaglutide 0.1 mg | 1.07 |
| Semaglutide 0.2 mg | 1.08 |
| Semaglutide 0.4 mg | 0.99 |
| Placebo | 1.04 |
Change in NFS from baseline to week 72 is presented. NFS is calculated using formula: NFS = -1.675 + 0.037 * age (years) + 0.094 * body mass index (BMI) (kg/m^2) + 1.13 * hyperglycaemia (yes/no) + 0.99 * Aspartate aminotransferase (AST)/ Alanine aminotransferase (ALT) ratio + 0.013 × platelet count (*10^9/L) - 0.66 * albumin (g/dL). The score is used to classify the probability of fibrosis. A score a) < -1.5 indicates a low probability, b) > -1.5 to < 0.67 indicates intermediate probability, and a score of c) > 0.67 indicates a high probability of liver fibrosis. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Score on a scale (Mean) |
|---|---|
| Semaglutide 0.1 mg | -0.322 |
| Semaglutide 0.2 mg | -0.617 |
| Semaglutide 0.4 mg | -0.475 |
| Placebo | -0.040 |
Change in potassium (measured as mEq/L) is presented as ratio to baseline. The endpoint was evaluated based on the data from on-treatment period. On-treatment period: the period starting on the date of first administration of trial product and ending on the date of the last dose of trial product +7 days; except for the evaluation of AEs and hypoglycaemic episodes for which the period ended on the date of whatever came first: 1) last dose of trial product + 49 days (7 half-lives of semaglutide); 2) end of the in-trial period. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Ratio of potassium (Geometric Mean) |
|---|---|
| Semaglutide 0.1 mg | 1.004 |
| Semaglutide 0.2 mg | 0.979 |
| Semaglutide 0.4 mg | 0.998 |
| Placebo | 0.998 |
Change in potassium (measured as mmol/L) is presented as ratio to baseline. The endpoint was evaluated based on the data from on-treatment period. On-treatment period: the period starting on the date of first administration of trial product and ending on the date of the last dose of trial product +7 days; except for the evaluation of AEs and hypoglycaemic episodes for which the period ended on the date of whatever came first: 1) last dose of trial product + 49 days (7 half-lives of semaglutide); 2) end of the in-trial period. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Ratio of potassium (Geometric Mean) |
|---|---|
| Semaglutide 0.1 mg | 1.004 |
| Semaglutide 0.2 mg | 0.979 |
| Semaglutide 0.4 mg | 0.998 |
| Placebo | 0.998 |
Change in pulse from baseline to week 72 is presented. The endpoint was evaluated based on the data from on-treatment period. On-treatment period: the period starting on the date of first administration of trial product and ending on the date of the last dose of trial product +7 days; except for the evaluation of AEs and hypoglycaemic episodes for which the period ended on the date of whatever came first: 1) last dose of trial product + 49 days (7 half-lives of semaglutide); 2) end of the in-trial period. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | beats per minute (bpm) (Mean) |
|---|---|
| Semaglutide 0.1 mg | 2.2 |
| Semaglutide 0.2 mg | 2.1 |
| Semaglutide 0.4 mg | 0.9 |
| Placebo | -0.3 |
Change in sodium (measured as milli equivalent per liter (mEq/L)) is presented as ratio to baseline. The endpoint was evaluated based on the data from on-treatment period. On-treatment period: the period starting on the date of first administration of trial product and ending on the date of the last dose of trial product +7 days; except for the evaluation of AEs and hypoglycaemic episodes for which the period ended on the date of whatever came first: 1) last dose of trial product + 49 days (7 half-lives of semaglutide); 2) end of the in-trial period. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Ratio of sodium (Geometric Mean) |
|---|---|
| Semaglutide 0.1 mg | 0.999 |
| Semaglutide 0.2 mg | 1.000 |
| Semaglutide 0.4 mg | 1.002 |
| Placebo | 1.002 |
Change in sodium (measured as milli mole per liter (mmol/L)) is presented as ratio to baseline. The endpoint was evaluated based on the data from on-treatment period. On-treatment period: the period starting on the date of first administration of trial product and ending on the date of the last dose of trial product +7 days; except for the evaluation of AEs and hypoglycaemic episodes for which the period ended on the date of whatever came first: 1) last dose of trial product + 49 days (7 half-lives of semaglutide); 2) end of the in-trial period. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Ratio of sodium (Geometric Mean) |
|---|---|
| Semaglutide 0.1 mg | 0.999 |
| Semaglutide 0.2 mg | 1.000 |
| Semaglutide 0.4 mg | 1.002 |
| Placebo | 1.002 |
Blood pressure was measured in a sitting position after 5 minutes of rest. Change in SBP from baseline to week 72 is presented. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Millimeters of mercury (Mean) |
|---|---|
| Semaglutide 0.1 mg | -2 |
| Semaglutide 0.2 mg | -7 |
| Semaglutide 0.4 mg | -6 |
| Placebo | -2 |
Change in thrombocytes from baseline to week 72 is presented. The endpoint was evaluated based on the data from on-treatment period. On-treatment period: the period starting on the date of first administration of trial product and ending on the date of the last dose of trial product +7 days; except for the evaluation of AEs and hypoglycaemic episodes for which the period ended on the date of whatever came first: 1) last dose of trial product + 49 days (7 half-lives of semaglutide); 2) end of the in-trial period. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | 10^9 cells per liter (10^9/L) (Mean) |
|---|---|
| Semaglutide 0.1 mg | 8.8 |
| Semaglutide 0.2 mg | 14.6 |
| Semaglutide 0.4 mg | 9.0 |
| Placebo | 0.3 |
Change in total bilirubin (measured as milligram per deciliter (mg/dL)) is presented as ratio to baseline. The endpoint was evaluated based on the data from on-treatment period. On-treatment period: the period starting on the date of first administration of trial product and ending on the date of the last dose of trial product +7 days; except for the evaluation of AEs and hypoglycaemic episodes for which the period ended on the date of whatever came first: 1) last dose of trial product + 49 days (7 half-lives of semaglutide); 2) end of the in-trial period. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Ratio of total bilirubin (Geometric Mean) |
|---|---|
| Semaglutide 0.1 mg | 0.978 |
| Semaglutide 0.2 mg | 1.011 |
| Semaglutide 0.4 mg | 0.949 |
| Placebo | 1.040 |
Change in total bilirubin (measured as micromole per liter (umol/L)) is presented as ratio to baseline. The endpoint was evaluated based on the data from on-treatment period. On-treatment period: the period starting on the date of first administration of trial product and ending on the date of the last dose of trial product +7 days; except for the evaluation of AEs and hypoglycaemic episodes for which the period ended on the date of whatever came first: 1) last dose of trial product + 49 days (7 half-lives of semaglutide); 2) end of the in-trial period. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Ratio of total bilirubin (Geometric Mean) |
|---|---|
| Semaglutide 0.1 mg | 0.978 |
| Semaglutide 0.2 mg | 1.011 |
| Semaglutide 0.4 mg | 0.949 |
| Placebo | 1.040 |
Change in total cholesterol (measured as millimoles per liter) is presented as ratio to baseline. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Ratio of total cholesterol (Geometric Mean) |
|---|---|
| Semaglutide 0.1 mg | 0.98 |
| Semaglutide 0.2 mg | 1.00 |
| Semaglutide 0.4 mg | 0.93 |
| Placebo | 0.93 |
Change in triglycerides (measured as millimoles per liter) is presented as ratio to baseline. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Ratio of triglycerides (Geometric Mean) |
|---|---|
| Semaglutide 0.1 mg | 0.88 |
| Semaglutide 0.2 mg | 0.89 |
| Semaglutide 0.4 mg | 0.73 |
| Placebo | 0.95 |
Change in urea (measured as milli mole per liter) is presented as ratio to baseline. The endpoint was evaluated based on the data from on-treatment period. On-treatment period: the period starting on the date of first administration of trial product and ending on the date of the last dose of trial product +7 days; except for the evaluation of AEs and hypoglycaemic episodes for which the period ended on the date of whatever came first: 1) last dose of trial product + 49 days (7 half-lives of semaglutide); 2) end of the in-trial period. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Ratio of urea (Geometric Mean) |
|---|---|
| Semaglutide 0.1 mg | 1.018 |
| Semaglutide 0.2 mg | 0.973 |
| Semaglutide 0.4 mg | 1.042 |
| Placebo | 1.043 |
Change in VLDL cholesterol (measured as millimoles per liter) is presented as ratio to baseline. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Ratio of VLDL cholesterol (Geometric Mean) |
|---|---|
| Semaglutide 0.1 mg | 0.89 |
| Semaglutide 0.2 mg | 0.90 |
| Semaglutide 0.4 mg | 0.74 |
| Placebo | 0.93 |
Change in waist circumference from baseline to week 72 is presented. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Centimeters (Mean) |
|---|---|
| Semaglutide 0.1 mg | -3.9 |
| Semaglutide 0.2 mg | -7.1 |
| Semaglutide 0.4 mg | -11.4 |
| Placebo | -1.7 |
Number of participants discontinuing treatment due to gastrointestinal adverse events is presented. The endpoint was evaluated based on the data from on-treatment period. On-treatment period: the period starting on the date of first administration of trial product and ending on the date of the last dose of trial product +7 days; except for the evaluation of AEs and hypoglycaemic episodes for which the period ended on the date of whatever came first: 1) last dose of trial product + 49 days (7 half-lives of semaglutide); 2) end of the in-trial period. (NCT02970942)
Timeframe: From week 0 to week 79
| Intervention | Participants (Count of Participants) |
|---|---|
| Semaglutide 0.1 mg | 1 |
| Semaglutide 0.2 mg | 6 |
| Semaglutide 0.4 mg | 2 |
| Placebo | 0 |
An adverse event (AE) was any untoward medical occurrence in a clinical trial participant administered or using a medicinal product, whether or not considered related to the medicinal product or usage. All AEs reported here are TEAEs. TEAE is defined as an event that had onset date during the on-treatment period. The endpoint was evaluated based on the data from on-treatment period. On-treatment period: the period starting on the date of first administration of trial product and ending on the date of the last dose of trial product +7 days; except for the evaluation of AEs and hypoglycaemic episodes for which the period ended on the date of whatever came first: 1) last dose of trial product + 49 days (7 half lives of semaglutide); 2) end of the in-trial period. (NCT02970942)
Timeframe: From week 0 to week 79
| Intervention | events (Number) |
|---|---|
| Semaglutide 0.1 mg | 525 |
| Semaglutide 0.2 mg | 577 |
| Semaglutide 0.4 mg | 511 |
| Placebo | 445 |
Hypoglycaemic episode (blood glucose less than or equal to (<=) 3.9 mmol/L (70 mg/dL) Or greater than (>) 3.9 mmol/L (70 mg/dL) occurring in conjunction with hypoglycaemic symptoms) is defined as treatment emergent if the onset of the episode occurs during the on-treatment period. On-treatment period: the period starting on the date of first administration of trial product and ending on the date of the last dose of trial product +7 days; except for the evaluation of AEs and hypoglycaemic episodes for which the period ended on the date of whatever came first: 1) last dose of trial product + 49 days (7 half-lives of semaglutide); 2) end of the in-trial period. (NCT02970942)
Timeframe: From week 0 to week 79
| Intervention | episodes (Number) |
|---|---|
| Semaglutide 0.1 mg | 54 |
| Semaglutide 0.2 mg | 30 |
| Semaglutide 0.4 mg | 66 |
| Placebo | 18 |
Severe hypoglycaemia: An episode requiring assistance of another person to actively administer carbohydrate, glucagon, or take other corrective actions. Plasma glucose concentrations may not be available during an event, but neurological recovery following the return of plasma glucose to normal is considered sufficient evidence that the event was induced by a low plasma glucose concentration. Hypoglycaemic episode is defined as treatment emergent if the onset of the episode occurs during the on-treatment period. On-treatment period: the period starting on the date of first administration of trial product and ending on the date of the last dose of trial product +7 days; except for the evaluation of AEs and hypoglycaemic episodes for which the period ended on the date of whatever came first: 1) last dose of trial product + 49 days (7 half-lives of semaglutide); 2) end of the in-trial period. (NCT02970942)
Timeframe: From week 0 to week 79
| Intervention | episodes (Number) |
|---|---|
| Semaglutide 0.1 mg | 2 |
| Semaglutide 0.2 mg | 2 |
| Semaglutide 0.4 mg | 0 |
| Placebo | 0 |
Severe or BG confirmed symptomatic hypoglycaemia: episode, severe as per american diabetes association (ADA) classification or BG confirmed by plasma glucose value < 3.1 mmol/L(56mg/dL) with symptoms along with hypoglycaemia. Severe hypoglycaemia: episode requiring assistance of other person to actively administer carbohydrate, glucagon, or take corrective actions. Plasma glucose concentrations may not be available during event, but neurological recovery following return of plasma glucose to normal is sufficient evidence that event was induced by low plasma glucose concentration. Hypoglycaemic episode is treatment emergent if onset of it occurs during on-treatment period: period starting on day of first administration of trial product and ending on day of last dose of trial product+7 days; except for evaluation of AEs; hypoglycaemic episodes for which period ended on date of whatever came first:last dose of trial product + 49 days (7 half-lives of semaglutide); end of in-trial period. (NCT02970942)
Timeframe: From week 0 to week 79
| Intervention | episodes (Number) |
|---|---|
| Semaglutide 0.1 mg | 3 |
| Semaglutide 0.2 mg | 5 |
| Semaglutide 0.4 mg | 17 |
| Placebo | 2 |
Change in CK-18 fragments (M30, M65) (measured as units per liter) is presented as ratio to baseline. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Ratio of CK-18 fragments (Geometric Mean) | |
|---|---|---|
| M30 | M65 | |
| Placebo | 0.78 | 0.71 |
| Semaglutide 0.1 mg | 0.52 | 0.51 |
| Semaglutide 0.2 mg | 0.50 | 0.52 |
| Semaglutide 0.4 mg | 0.40 | 0.38 |
Change in SF-36 score from baseline to week 72 is presented. SF-36 measures participant's overall health related quality of life (HRQoL). It is a 36-item generic measure of health status and yields 2 summary scores for physical health and mental health, and 8 domain scores (physical functioning, role functioning, bodily pain, general health, vitality, social functioning, role emotional, mental health). The scores 0-100 (where higher scores indicates a better HRQoL) from the SF-36 were converted to norm-based scores to enable a direct interpretation in relation to the distribution of scores in the 2009 U.S. general population. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Scores on a scale (Mean) | |||||||||
|---|---|---|---|---|---|---|---|---|---|---|
| Mental component sum | Physical component sum | Physical functioning | Role functioning | Bodily pain | General health | Vitality | Social functioning | Role emotional | Mental health | |
| Placebo | -0.4 | -0.1 | -0.4 | -0.3 | -1.3 | 4.3 | -0.2 | -1.6 | -0.3 | -0.2 |
| Semaglutide 0.1 mg | 2.2 | 2.1 | 1.8 | 2.1 | 1.3 | 7.2 | 2.3 | 3.7 | 2.2 | 1.2 |
| Semaglutide 0.2 mg | 0.6 | 1.1 | 2.0 | 0.5 | 1.2 | 2.3 | 0.6 | -0.1 | 0.6 | 1.5 |
| Semaglutide 0.4 mg | 1.2 | 3.9 | 2.8 | 2.2 | 3.4 | 9.0 | 4.6 | 2.2 | 0.5 | 1.3 |
Number of participants with anti-semaglutide antibodies with in vitro neutralising effect during and after 72 weeks treatment is presented. In the below table, 'Yes' infers number of participants with anti-semaglutide antibodies with in vitro neutralising effect and 'No' infers number of participants without anti-semaglutide antibodies with in vitro neutralising effect during and after 72 weeks treatment. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: From week 0 to week 79
| Intervention | Participants (Count of Participants) | |
|---|---|---|
| Yes | No | |
| Semaglutide 0.1 mg | 0 | 80 |
| Semaglutide 0.2 mg | 0 | 78 |
| Semaglutide 0.4 mg | 0 | 81 |
Number of participants with anti-semaglutide binding antibodies cross reacting with native glucagon-like peptide-1 (GLP-1) during and after 72 weeks treatment is presented. In the below table, 'Yes' infers number of participants with anti-semaglutide antibodies cross reacting with native GLP-1 and 'No' infers number of participants without anti-semaglutide antibodies cross reacting with native GLP-1 during and after 72 weeks treatment. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: From week 0 to week 79
| Intervention | Participants (Count of Participants) | |
|---|---|---|
| Yes | No | |
| Semaglutide 0.1 mg | 4 | 76 |
| Semaglutide 0.2 mg | 0 | 78 |
| Semaglutide 0.4 mg | 2 | 79 |
Number of participants with cross-reacting anti-semaglutide binding antibodies with in vitro neutralising effect to native GLP-1 during and after 72 weeks treatment is presented. In the below table, 'Yes' infers number of participants with cross-reacting anti-semaglutide binding antibodies with in vitro neutralising effect to native GLP-1 and 'No' infers number of participants without cross-reacting anti-semaglutide binding antibodies with in vitro neutralising effect to native GLP-1 during and after 72 weeks treatment. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: From week 0 to week 79
| Intervention | Participants (Count of Participants) | |
|---|---|---|
| Yes | No | |
| Semaglutide 0.1 mg | 0 | 80 |
| Semaglutide 0.2 mg | 0 | 78 |
| Semaglutide 0.4 mg | 0 | 81 |
Number of participants with occurrence of anti-semaglutide antibodies during and after 72 weeks treatment is presented. In the below table, 'Yes' infers number of participants with occurrence of anti-semaglutide antibodies and 'No' infers number of participants without anti-semaglutide antibodies during and after 72 weeks treatment. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: From week 0 to week 79
| Intervention | Participants (Count of Participants) | |
|---|---|---|
| Yes | No | |
| Semaglutide 0.1 mg | 4 | 76 |
| Semaglutide 0.2 mg | 1 | 77 |
| Semaglutide 0.4 mg | 2 | 79 |
NASH resolution defined by NASH clinical research network as lobular inflammation of 0 or 1; hepatocellular ballooning reduced to 0; both criteria were necessary conditions. Hepatocellular ballooning range: 0-2; lobular inflammation range: 0-3, with higher scores indicating more severe hepatocellular ballooning or lobular inflammation. Worsening of fibrosis defined by an increase in fibrosis at least one stage of Kleiner fibrosis classification: fibrosis stages range from 0-4, higher scores indicate greater fibrosis (0=None, 4=Cirrhosis). Endpoint was evaluated based on data from in-trial period which started on date of randomisation visit and ended on first of following dates (both inclusive):1) follow-up visit (Week 79); 2) withdrawal of consent; 3)last contact with participant (for participants lost to follow-up); 4)death. (NCT02970942)
Timeframe: After 72 weeks
| Intervention | Percentage of participants (Number) | ||
|---|---|---|---|
| Yes | No | Missing | |
| Placebo | 32.8 | 58.6 | 8.6 |
| Semaglutide 0.1 mg | 49.1 | 45.6 | 5.3 |
| Semaglutide 0.2 mg | 32.2 | 50.8 | 16.9 |
| Semaglutide 0.4 mg | 42.9 | 46.4 | 10.7 |
Percentage of participants who had improved, worsened, or had no change in the activity component of the SAF score from baseline to week 72 is presented. SAF score was assessed on a scale of 0-4, with higher scores indicating more severe disease. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Percentage of participants (Number) | |||
|---|---|---|---|---|
| Improvement | Worsening | No change | Missing | |
| Placebo | 42.5 | 11.3 | 33.8 | 12.5 |
| Semaglutide 0.1 mg | 62.5 | 7.5 | 22.5 | 7.5 |
| Semaglutide 0.2 mg | 71.8 | 3.8 | 11.5 | 12.8 |
| Semaglutide 0.4 mg | 72.0 | 1.2 | 14.6 | 12.2 |
A 12-lead ECG was performed at baseline (week 0) and week 72 and categorised as normal, abnormal and not clinically significant (abnormal NCS) or abnormal and clinically significant (abnormal CS). Percentage of participants in each ECG category at week 0 and week 72 are presented. The endpoint was evaluated based on the data from on-treatment period. On-treatment period: the period starting on the date of first administration of trial product and ending on the date of the last dose of trial product +7 days; except for the evaluation of AEs and hypoglycaemic episodes for which the period ended on the date of whatever came first: 1) last dose of trial product + 49 days (7 half-lives of semaglutide); 2) end of the in-trial period. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Percentage of participants (Number) | |||||
|---|---|---|---|---|---|---|
| Week 0: Normal | Week 0: Abnormal NCS | Week 0: Abnormal CS | Week 72: Normal | Week 72: Abnormal NCS | Week 72: Abnormal CS | |
| Placebo | 63.8 | 36.3 | 0.0 | 60.0 | 38.6 | 1.4 |
| Semaglutide 0.1 mg | 58.8 | 41.3 | 0.0 | 64.9 | 35.1 | 0.0 |
| Semaglutide 0.2 mg | 60.3 | 39.7 | 0.0 | 65.1 | 34.9 | 0.0 |
| Semaglutide 0.4 mg | 66.7 | 32.1 | 1.2 | 74.6 | 23.9 | 1.4 |
Percentage of participants who had improved, worsened, or had no change in fibrosis stage from baseline to week 72 is presented. The degree of fibrosis is described by the Kleiner fibrosis staging system, ranging from F0 (absence of fibrosis), F1 (portal/perisinusoidal fibrosis), F2 (perisinusoidal and portal/periportal fibrosis), F3 (septal or bridging fibrosis) through F4 (cirrhosis). The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Percentage of participants (Number) | |||
|---|---|---|---|---|
| Improvement | Worsening | No change | Missing | |
| Placebo | 31.3 | 18.8 | 37.5 | 12.5 |
| Semaglutide 0.1 mg | 46.3 | 10.0 | 36.3 | 7.5 |
| Semaglutide 0.2 mg | 32.1 | 7.7 | 42.3 | 17.9 |
| Semaglutide 0.4 mg | 42.7 | 4.9 | 36.6 | 15.9 |
Percentage of participants who had improved, worsened, or had no change in hepatocyte ballooning from baseline to week 72 is presented. Hepatocyte ballooning was assessed on a scale of 0-2, with higher scores indicating more severe disease. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Percentage of participants (Number) | |||
|---|---|---|---|---|
| Improvement | Worsening | No change | Missing | |
| Placebo | 38.8 | 2.5 | 46.3 | 12.5 |
| Semaglutide 0.1 mg | 61.3 | 2.5 | 28.8 | 7.5 |
| Semaglutide 0.2 mg | 70.5 | 2.6 | 14.1 | 12.8 |
| Semaglutide 0.4 mg | 74.4 | 1.2 | 12.2 | 12.2 |
Percentage of participants who had improved, worsened, or had no change in lobular inflammation from baseline to week 72 is presented. Lobular inflammation was assessed on a scale of 0-3, with higher scores indicating more severe lobular inflammation. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Percentage of participants (Number) | |||
|---|---|---|---|---|
| Improvement | Worsening | No change | Missing | |
| Placebo | 26.3 | 17.5 | 45.0 | 11.3 |
| Semaglutide 0.1 mg | 41.3 | 7.5 | 43.8 | 7.5 |
| Semaglutide 0.2 mg | 47.4 | 7.7 | 32.1 | 12.8 |
| Semaglutide 0.4 mg | 37.8 | 6.1 | 43.9 | 12.2 |
Percentage of participants with change in physical examination (cardiovascular system) from week -6 to week 72 is presented. The endpoint was evaluated based on the data from on-treatment period. On-treatment period: the period starting on the date of first administration of trial product and ending on the date of the last dose of trial product +7 days; except for the evaluation of AEs and hypoglycaemic episodes for which the period ended on the date of whatever came first: 1) last dose of trial product + 49 days (7 half-lives of semaglutide); 2) end of the in-trial period. (NCT02970942)
Timeframe: Week -6, week 72
| Intervention | Percentage of participants (Number) | |||||
|---|---|---|---|---|---|---|
| Week -6: Normal | Week -6: Abnormal NCS | Week -6: Abnormal CS | Week 72: Normal | Week 72: Abnormal NCS | Week 72: Abnormal CS | |
| Placebo | 92.5 | 6.3 | 1.3 | 90.1 | 8.5 | 1.4 |
| Semaglutide 0.1 mg | 87.5 | 11.3 | 1.3 | 87.8 | 12.2 | 0.0 |
| Semaglutide 0.2 mg | 93.6 | 5.1 | 1.3 | 96.9 | 3.1 | 0.0 |
| Semaglutide 0.4 mg | 92.6 | 7.4 | 0.0 | 94.4 | 5.6 | 0.0 |
Percentage of participants with change in physical examination (central and peripheral nervous system) from week -6 to week 72 is presented. The endpoint was evaluated based on the data from on-treatment period. On-treatment period: the period starting on the date of first administration of trial product and ending on the date of the last dose of trial product +7 days; except for the evaluation of AEs and hypoglycaemic episodes for which the period ended on the date of whatever came first: 1) last dose of trial product + 49 days (7 half-lives of semaglutide); 2) end of the in-trial period. (NCT02970942)
Timeframe: Week -6, week 72
| Intervention | Percentage of participants (Number) | |||||
|---|---|---|---|---|---|---|
| Week -6: Normal | Week -6: Abnormal NCS | Week -6: Abnormal CS | Week 72: Normal | Week 72: Abnormal NCS | Week 72: Abnormal CS | |
| Placebo | 95.0 | 3.8 | 1.3 | 92.9 | 7.1 | 0.0 |
| Semaglutide 0.1 mg | 92.5 | 5.0 | 2.5 | 94.6 | 5.4 | 0.0 |
| Semaglutide 0.2 mg | 94.8 | 5.2 | 0.0 | 93.7 | 4.8 | 1.6 |
| Semaglutide 0.4 mg | 98.7 | 1.3 | 0.0 | 98.6 | 1.4 | 0.0 |
Percentage of participants with change in physical examination (gastrointestinal system including mouth) from week -6 to week 72 is presented. The endpoint was evaluated based on the data from on-treatment period. On-treatment period: the period starting on the date of first administration of trial product and ending on the date of the last dose of trial product +7 days; except for the evaluation of AEs and hypoglycaemic episodes for which the period ended on the date of whatever came first: 1) last dose of trial product + 49 days (7 half-lives of semaglutide); 2) end of the in-trial period. (NCT02970942)
Timeframe: Week -6, week 72
| Intervention | Percentage of participants (Number) | |||||
|---|---|---|---|---|---|---|
| Week -6: Normal | Week -6: Abnormal NCS | Week -6: Abnormal CS | Week 72: Normal | Week 72: Abnormal NCS | Week 72: Abnormal CS | |
| Placebo | 86.3 | 12.5 | 1.3 | 84.5 | 14.1 | 1.4 |
| Semaglutide 0.1 mg | 82.5 | 13.8 | 3.8 | 89.2 | 10.8 | 0.0 |
| Semaglutide 0.2 mg | 83.1 | 15.6 | 1.3 | 81.0 | 19.0 | 0.0 |
| Semaglutide 0.4 mg | 84.0 | 16.0 | 0.0 | 87.5 | 12.5 | 0.0 |
Percentage of participants with change in physical examination (general appearance) from week -6 to week 72 is presented. The endpoint was evaluated based on the data from on-treatment period. On-treatment period: the period starting on the date of first administration of trial product and ending on the date of the last dose of trial product +7 days; except for the evaluation of AEs and hypoglycaemic episodes for which the period ended on the date of whatever came first: 1) last dose of trial product + 49 days (7 half-lives of semaglutide); 2) end of the in-trial period. (NCT02970942)
Timeframe: Week -6, week 72
| Intervention | Percentage of participants (Number) | |||||
|---|---|---|---|---|---|---|
| Week -6: Normal | Week -6: Abnormal NCS | Week -6: Abnormal CS | Week 72: Normal | Week 72: Abnormal NCS | Week 72: Abnormal CS | |
| Placebo | 80.0 | 20.0 | 0.0 | 76.1 | 23.9 | 0.0 |
| Semaglutide 0.1 mg | 83.8 | 16.3 | 0.0 | 83.8 | 16.2 | 0.0 |
| Semaglutide 0.2 mg | 85.9 | 12.8 | 1.3 | 90.6 | 6.3 | 3.1 |
| Semaglutide 0.4 mg | 79.0 | 21.0 | 0.0 | 90.3 | 9.7 | 0.0 |
Percentage of participants with change in physical examination (head, ears, eyes, nose, throat, neck) from week -6 to week 72 is presented. The endpoint was evaluated based on the data from on-treatment period. On-treatment period: the period starting on the date of first administration of trial product and ending on the date of the last dose of trial product +7 days; except for the evaluation of AEs and hypoglycaemic episodes for which the period ended on the date of whatever came first: 1) last dose of trial product + 49 days (7 half-lives of semaglutide); 2) end of the in-trial period. (NCT02970942)
Timeframe: Week -6, week 72
| Intervention | Percentage of participants (Number) | |||||
|---|---|---|---|---|---|---|
| Week -6: Normal | Week -6: Abnormal NCS | Week -6: Abnormal CS | Week 72: Normal | Week 72: Abnormal NCS | Week 72: Abnormal CS | |
| Placebo | 97.5 | 2.5 | 0.0 | 98.6 | 0.0 | 1.4 |
| Semaglutide 0.1 mg | 97.5 | 2.5 | 0.0 | 94.5 | 4.1 | 1.4 |
| Semaglutide 0.2 mg | 94.8 | 5.2 | 0.0 | 96.8 | 3.2 | 0.0 |
| Semaglutide 0.4 mg | 98.8 | 1.3 | 0.0 | 98.6 | 1.4 | 0.0 |
Percentage of participants with change in physical examination (lymph node palpation) from week -6 to week 72 is presented. The endpoint was evaluated based on the data from on-treatment period. On-treatment period: the period starting on the date of first administration of trial product and ending on the date of the last dose of trial product +7 days; except for the evaluation of AEs and hypoglycaemic episodes for which the period ended on the date of whatever came first: 1) last dose of trial product + 49 days (7 half-lives of semaglutide); 2) end of the in-trial period. (NCT02970942)
Timeframe: Week -6, week 72
| Intervention | Percentage of participants (Number) | |||||
|---|---|---|---|---|---|---|
| Week -6: Normal | Week -6: Abnormal NCS | Week -6: Abnormal CS | Week 72: Normal | Week 72: Abnormal NCS | Week 72: Abnormal CS | |
| Placebo | 100.0 | 0.0 | 0.0 | 100.0 | 0.0 | 0.0 |
| Semaglutide 0.1 mg | 100.0 | 0.0 | 0.0 | 100.0 | 0.0 | 0.0 |
| Semaglutide 0.2 mg | 98.7 | 1.3 | 0.0 | 100.0 | 0.0 | 0.0 |
| Semaglutide 0.4 mg | 100.0 | 0.0 | 0.0 | 100.0 | 0.0 | 0.0 |
Percentage of participants with change in physical examination (musculoskeletal system) from week -6 to week 72 is presented. The endpoint was evaluated based on the data from on-treatment period. On-treatment period: the period starting on the date of first administration of trial product and ending on the date of the last dose of trial product +7 days; except for the evaluation of AEs and hypoglycaemic episodes for which the period ended on the date of whatever came first: 1) last dose of trial product + 49 days (7 half-lives of semaglutide); 2) end of the in-trial period. (NCT02970942)
Timeframe: Week -6, week 72
| Intervention | Percentage of participants (Number) | |||||
|---|---|---|---|---|---|---|
| Week -6: Normal | Week -6: Abnormal NCS | Week -6: Abnormal CS | Week 72: Normal | Week 72: Abnormal NCS | Week 72: Abnormal CS | |
| Placebo | 95.0 | 3.8 | 1.3 | 95.8 | 4.2 | 0.0 |
| Semaglutide 0.1 mg | 95.0 | 3.8 | 1.3 | 94.6 | 5.4 | 0.0 |
| Semaglutide 0.2 mg | 96.1 | 3.9 | 0.0 | 96.8 | 3.2 | 0.0 |
| Semaglutide 0.4 mg | 94.9 | 5.1 | 0.0 | 100.0 | 0.0 | 0.0 |
Percentage of participants with change in physical examination (respiratory system) from week -6 to week 72 is presented. The endpoint was evaluated based on the data from on-treatment period. On-treatment period: the period starting on the date of first administration of trial product and ending on the date of the last dose of trial product +7 days; except for the evaluation of AEs and hypoglycaemic episodes for which the period ended on the date of whatever came first: 1) last dose of trial product + 49 days (7 half-lives of semaglutide); 2) end of the in-trial period. (NCT02970942)
Timeframe: Week -6, week 72
| Intervention | Percentage of participants (Number) | |||||
|---|---|---|---|---|---|---|
| Week -6: Normal | Week -6: Abnormal NCS | Week -6: Abnormal CS | Week 72: Normal | Week 72: Abnormal NCS | Week 72: Abnormal CS | |
| Placebo | 97.5 | 2.5 | 0.0 | 98.6 | 1.4 | 0.0 |
| Semaglutide 0.1 mg | 100.0 | 0.0 | 0.0 | 98.6 | 0.0 | 1.4 |
| Semaglutide 0.2 mg | 100.0 | 0.0 | 0.0 | 96.9 | 3.1 | 0.0 |
| Semaglutide 0.4 mg | 100.0 | 0.0 | 0.0 | 98.6 | 1.4 | 0.0 |
Percentage of participants with change in physical examination (skin) from week -6 to week 72 is presented. The endpoint was evaluated based on the data from on-treatment period. On-treatment period: the period starting on the date of first administration of trial product and ending on the date of the last dose of trial product +7 days; except for the evaluation of AEs and hypoglycaemic episodes for which the period ended on the date of whatever came first: 1) last dose of trial product + 49 days (7 half-lives of semaglutide); 2) end of the in-trial period. (NCT02970942)
Timeframe: Week -6, week 72
| Intervention | Percentage of participants (Number) | |||||
|---|---|---|---|---|---|---|
| Week -6: Normal | Week -6: Abnormal NCS | Week -6: Abnormal CS | Week 72: Normal | Week 72: Abnormal NCS | Week 72: Abnormal CS | |
| Placebo | 90.0 | 10.0 | 0.0 | 88.7 | 11.3 | 0.0 |
| Semaglutide 0.1 mg | 96.3 | 2.5 | 1.3 | 94.6 | 4.1 | 1.4 |
| Semaglutide 0.2 mg | 92.3 | 6.4 | 1.3 | 87.5 | 10.9 | 1.6 |
| Semaglutide 0.4 mg | 85.2 | 13.6 | 1.2 | 90.0 | 8.6 | 1.4 |
Percentage of participants with change in physical examination (thyroid gland) from week -6 to week 72 is presented. The endpoint was evaluated based on the data from on-treatment period. On-treatment period: the period starting on the date of first administration of trial product and ending on the date of the last dose of trial product +7 days; except for the evaluation of AEs and hypoglycaemic episodes for which the period ended on the date of whatever came first: 1) last dose of trial product + 49 days (7 half-lives of semaglutide); 2) end of the in-trial period. (NCT02970942)
Timeframe: Week -6, week 72
| Intervention | Percentage of participants (Number) | |||||
|---|---|---|---|---|---|---|
| Week -6: Normal | Week -6: Abnormal NCS | Week -6: Abnormal CS | Week 72: Normal | Week 72: Abnormal NCS | Week 72: Abnormal CS | |
| Placebo | 98.8 | 0.0 | 1.3 | 98.6 | 1.4 | 0.0 |
| Semaglutide 0.1 mg | 88.8 | 10.0 | 1.3 | 94.6 | 5.4 | 0.0 |
| Semaglutide 0.2 mg | 97.4 | 2.6 | 0.0 | 98.4 | 1.6 | 0.0 |
| Semaglutide 0.4 mg | 97.5 | 2.5 | 0.0 | 97.1 | 2.9 | 0.0 |
Percentage of participants who had improved, worsened, or had no change in steatosis from baseline to week 72 is presented. Steatosis was assessed on a scale of 0-3, with higher scores indicating more severe steatosis. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Percentage of participants (Number) | |||
|---|---|---|---|---|
| Improvement | Worsening | No change | Missing | |
| Placebo | 26.3 | 15.0 | 46.3 | 12.5 |
| Semaglutide 0.1 mg | 52.5 | 6.3 | 33.8 | 7.5 |
| Semaglutide 0.2 mg | 60.3 | 2.6 | 24.4 | 12.8 |
| Semaglutide 0.4 mg | 63.4 | 3.7 | 20.7 | 12.2 |
Percentage of participants who had worsened, improved or had no change in total NAS from baseline to week 72 is presented. Worsening is defined as an increase of at least 1 in the NAS; Improvement is defined as a decrease of at least 1 in the NAS; while no change corresponds to no change in NAS from baseline to week 72. NAS is calculated as the sum of scores for steatosis (0 to 3), lobular inflammation (0 to 3), and hepatocyte ballooning (0 to 2). Therefore, it is assessed on a scale of 0-8, with higher scores indicating more severe disease. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: Baseline (week 0), Week 72
| Intervention | Percentage of participants (Number) | |||
|---|---|---|---|---|
| Improvement | Worsening | No change | Missing | |
| Placebo | 43.8 | 16.3 | 27.5 | 12.5 |
| Semaglutide 0.1 mg | 71.3 | 7.5 | 13.8 | 7.5 |
| Semaglutide 0.2 mg | 79.5 | 2.6 | 5.1 | 12.8 |
| Semaglutide 0.4 mg | 82.9 | 3.7 | 1.2 | 12.2 |
NASH resolution defined by NASH clinical research network as lobular inflammation of 0 or 1 and hepatocellular ballooning reduced to 0; both criteria were necessary conditions. Hepatocellular ballooning ranges from 0-2; lobular inflammation ranges from 0-3, with higher scores indicating more severe hepatocellular ballooning or lobular inflammation. Worsening of fibrosis defined by an increase in fibrosis at least one stage of Kleiner fibrosis classification: fibrosis stages range from 0-4, with higher scores indicating greater fibrosis (0=None, 4=Cirrhosis). Endpoint was evaluated based on data from in-trial period which started on date of randomisation visit and ended on first of following dates (both inclusive):1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. (NCT02970942)
Timeframe: After 72 weeks
| Intervention | Percentage of participants (Number) | ||
|---|---|---|---|
| Yes | No | Missing | |
| Placebo | 17.2 | 74.1 | 8.6 |
| Semaglutide 0.1 mg | 40.4 | 54.4 | 5.3 |
| Semaglutide 0.2 mg | 35.6 | 47.5 | 16.9 |
| Semaglutide 0.4 mg | 58.9 | 30.4 | 10.7 |
Pentage of participants with weight loss of ≥ 10% of baseline body weight at 72 weeks is presented. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. In the below table, 'Yes' infers percentage of participants who have achieved ≥ 10% weight loss; 'No' infers percentage of participants who have not achieved ≥ 10% weight loss at 72 weeks and 'Missing' refers to percentage of participants with data missing due to different reasons (lost to follow-up, withdrawal). (NCT02970942)
Timeframe: Week 72
| Intervention | Percentage of participants (Number) | ||
|---|---|---|---|
| Yes | No | Missing | |
| Placebo | 2.5 | 92.5 | 5.0 |
| Semaglutide 0.1 mg | 17.5 | 77.5 | 5.0 |
| Semaglutide 0.2 mg | 38.5 | 52.6 | 9.0 |
| Semaglutide 0.4 mg | 59.8 | 34.1 | 6.1 |
Percentage of participants with weight loss of greater than or equal to (≥) 5% of baseline body weight at 72 weeks is presented. The endpoint was evaluated based on the data from in-trial period which started on the date of the randomisation visit and ended on the first of the following dates (both inclusive): 1) follow-up visit (Week 79); 2) withdrawal of consent; 3) last contact with participant (for participants lost to follow-up); 4) death. In the below table, 'Yes' infers percentage of participants who have achieved ≥ 5% weight loss; 'No' infers percentage of participants who have not achieved ≥ 5% weight loss at 72 weeks and 'Missing' refers to percentage of participants with data missing due to different reasons (lost to follow-up, withdrawal). (NCT02970942)
Timeframe: Week 72
| Intervention | Percentage of participants (Number) | ||
|---|---|---|---|
| Yes | No | Missing | |
| Placebo | 16.3 | 78.8 | 5.0 |
| Semaglutide 0.1 mg | 43.8 | 51.3 | 5.0 |
| Semaglutide 0.2 mg | 62.8 | 28.2 | 9.0 |
| Semaglutide 0.4 mg | 76.8 | 17.1 | 6.1 |
The Liver Fibrosis Score is an algorithmically derived score of liver fibrosis comprising measurements of tissue matrix metalloproteinase-1 (TIMP-1), hyaluronic acid (HA) and the amino terminal end of procollagen III (PIIINP) (see Guha et al. in Reference section). The Score represents a number on a numerical scale from 0 to 20. High values of the score (measured in arbitrary units) indicate high probability of advanced liver fibrosis, low scores indicate low probability of advanced liver fibrosis. Change in Liver Fibrosis Score was used to test the intervention. Change in liver fibrosis score represented the change in measurement as calculated as the arithmetic difference between the end value minus the baseline value of the Liver Fibrosis Score. The change in Liver Fibrosis Score can therefore be negative (representing an improvement in liver fibrosis between baseline and end of study) or be positive, (representing a worsening a liver fibrosis between baseline and end of study. (NCT00760513)
Timeframe: Baseline and 18 months
| Intervention | score on a scale (Mean) |
|---|---|
| Omega 3 Fatty Acid (Fish Oil) | 0.3 |
| Dummy Pill | 0.2 |
The NAFLD fibrosis score represented a validated algorithmically-derived measure of liver fibrosis as reported in Angulo et al (see reference section). The Score is derived from anthropometric and biochemical measurements in subjects. The NAFLD fibrosis score represents an arbitrary number with no units from -5.0 to +5.0. High positive NAFLD fibrosis scores indicate a high probability of advanced liver fibrosis. Negative scores represent a low probability of advanced liver fibrosis. The change in NAFLD fibrosis score (measured in arbitrary units) was used to test the effect of the intervention and represented the arithmetic difference in the end minus baseline measurements of this score. Thus, a negative change in the Score in the Table represented an improvement in liver fibrosis score between baseline and the end of the study. A positive change in the Score in the Table represented a worsening in liver fibrosis score between baseline and end of the study. (NCT00760513)
Timeframe: Baseline and 18 months
| Intervention | score on a scale (Mean) |
|---|---|
| Omega 3 Fatty Acid (Fish Oil) | 0.8 |
| Dummy Pill | 0.8 |
Percentage of liver fat was measured using magnetic resonance spectroscopy at baseline and end of study. High percentage values indicate a lot of liver fat (scale from 0 to 100%). Change in liver fat percentage represented the arithmetical difference between end of study liver fat percentage minus baseline measurement of liver fat percentage change in liver fat percentage was used to test whether the intervention decreased liver fat percentage. A negative change value in liver fat percentage indicates a response to therapy. A positive change value indicates no response to therapy. (NCT00760513)
Timeframe: Baseline and 18 months
| Intervention | percentage of liver fat (Mean) |
|---|---|
| Omega 3 Fatty Acid (Fish Oil) | -7.9 |
| Dummy Pill | -4.6 |
76 reviews available for 1-anilino-8-naphthalenesulfonate and Non-alcoholic Fatty Liver Disease
| Article | Year |
|---|---|
Clinical practice advice on lifestyle modification in the management of nonalcoholic fatty liver disease in Japan: an expert review.
Topics: Genetic Predisposition to Disease; Humans; Japan; Life Style; Lipase; Membrane Proteins; Non-alcohol | 2021 |
PNPLA3 as a therapeutic target for fatty liver disease: the evidence to date.
Topics: Genetic Predisposition to Disease; Genotype; Humans; Lipase; Liver; Membrane Proteins; Non-alcoholic | 2021 |
Update on Non-Alcoholic Fatty Liver Disease-Associated Single Nucleotide Polymorphisms and Their Involvement in Liver Steatosis, Inflammation, and Fibrosis: A Narrative Review
Topics: Fibronectins; Fibrosis; Genetic Predisposition to Disease; Humans; Inflammation; Interleukin-6; Lipa | 2022 |
Associations of PNPLA3 rs738409 Polymorphism with Plasma Lipid Levels: A Systematic Review and Meta-Analysis.
Topics: Acyltransferases; Adult; Case-Control Studies; Child; Cholesterol; Genetic Predisposition to Disease | 2022 |
Genetic contributions to NAFLD: leveraging shared genetics to uncover systems biology.
Topics: 17-Hydroxysteroid Dehydrogenases; Acyltransferases; Adaptor Proteins, Signal Transducing; Carcinoma, | 2020 |
Non-alcoholic fatty liver disease and cardiovascular disease: assessing the evidence for causality.
Topics: Animals; Cardiovascular Diseases; Humans; Lipase; Membrane Proteins; Non-alcoholic Fatty Liver Disea | 2020 |
Risk of Kidney Dysfunction IN Nafld.
Topics: Comorbidity; Humans; Kidney Failure, Chronic; Lipase; Membrane Proteins; Non-alcoholic Fatty Liver D | 2020 |
Combined use of Genetic Polymorphisms and Elastographic Techniques in NAFLD: Fact or Fiction?
Topics: Acyltransferases; Biopsy; Elasticity Imaging Techniques; Humans; Lipase; Liver; Liver Cirrhosis; Mem | 2020 |
Effect of the patatin-like phospholipase domain containing 3 gene (PNPLA3) I148M polymorphism on the risk and severity of nonalcoholic fatty liver disease and metabolic syndromes: A meta-analysis of paediatric and adolescent individuals.
Topics: Adolescent; Child; Female; Genetic Predisposition to Disease; Humans; Lipase; Male; Membrane Protein | 2020 |
Toward Genetic Prediction of Nonalcoholic Fatty Liver Disease Trajectories: PNPLA3 and Beyond.
Topics: Animals; Genetic Predisposition to Disease; Genetic Variation; Genome-Wide Association Study; Humans | 2020 |
Molecular Mechanisms: Connections between Nonalcoholic Fatty Liver Disease, Steatohepatitis and Hepatocellular Carcinoma.
Topics: 17-Hydroxysteroid Dehydrogenases; Animals; Apoptosis; Carcinoma, Hepatocellular; Diet, High-Fat; Dis | 2020 |
Epidemiology of nonalcoholic fatty liver disease in non-obese populations: Meta-analytic assessment of its prevalence, genetic, metabolic, and histological profiles.
Topics: Diabetes Mellitus; Humans; Lipase; Membrane Proteins; Metabolic Syndrome; Non-alcoholic Fatty Liver | 2020 |
APOC3rs2854116, PNPLA3rs738409, and TM6SF2rs58542926 polymorphisms might influence predisposition of NAFLD: A meta-analysis.
Topics: Apolipoprotein C-III; Female; Genetic Association Studies; Genetic Predisposition to Disease; Genoty | 2020 |
Genetics and epigenetics purpose in nonalcoholic fatty liver disease.
Topics: Acyltransferases; Adaptor Proteins, Signal Transducing; DNA Methylation; Epigenesis, Genetic; Histon | 2020 |
Association of PNPLA3 rs738409 G/C gene polymorphism with nonalcoholic fatty liver disease in children: a meta-analysis.
Topics: Child; Female; Genetic Association Studies; Genetic Predisposition to Disease; Humans; Lipase; Male; | 2020 |
A review of non-alcoholic fatty liver disease in non-obese and lean individuals.
Topics: Adiposity; Alleles; Diet, Healthy; Exercise; Female; Genetic Predisposition to Disease; Healthy Life | 2021 |
Nutrients, Genetic Factors, and Their Interaction in Non-Alcoholic Fatty Liver Disease and Cardiovascular Disease.
Topics: Apolipoproteins; Cardiovascular Diseases; Diet; Epigenesis, Genetic; Fatty Acids, Unsaturated; Fruct | 2020 |
Metabolic liver disease - what's in a name?
Topics: Adaptor Proteins, Signal Transducing; Colon; Dietary Sugars; Fructose; Genetic Predisposition to Dis | 2021 |
Nonalcoholic fatty liver disease or metabolic dysfunction-associated fatty liver disease diagnoses and cardiovascular diseases: From epidemiology to drug approaches.
Topics: Acyltransferases; Cardiovascular Diseases; Coronary Artery Disease; Diabetes Mellitus, Type 2; Dysli | 2021 |
NAFLD and renal function in children: is there a genetic link?
Topics: 17-Hydroxysteroid Dehydrogenases; Acyltransferases; Child; Humans; Lipase; Membrane Proteins; Non-al | 2021 |
The Role of Lipid Sensing Nuclear Receptors (PPARs and LXR) and Metabolic Lipases in Obesity, Diabetes and NAFLD.
Topics: Animals; Diabetes Mellitus; Humans; Lipase; Liver X Receptors; Non-alcoholic Fatty Liver Disease; Ob | 2021 |
Association between PNPLA3 rs738409 polymorphism and nonalcoholic fatty liver disease: a systematic review and meta-analysis.
Topics: Genetic Predisposition to Disease; Humans; Lipase; Membrane Proteins; Non-alcoholic Fatty Liver Dise | 2021 |
New trends on obesity and NAFLD in Asia.
Topics: Asia; Body Mass Index; Diet; Genetic Predisposition to Disease; Hepatitis B, Chronic; Humans; Incide | 2017 |
New trends on obesity and NAFLD in Asia.
Topics: Asia; Body Mass Index; Diet; Genetic Predisposition to Disease; Hepatitis B, Chronic; Humans; Incide | 2017 |
New trends on obesity and NAFLD in Asia.
Topics: Asia; Body Mass Index; Diet; Genetic Predisposition to Disease; Hepatitis B, Chronic; Humans; Incide | 2017 |
New trends on obesity and NAFLD in Asia.
Topics: Asia; Body Mass Index; Diet; Genetic Predisposition to Disease; Hepatitis B, Chronic; Humans; Incide | 2017 |
New trends on obesity and NAFLD in Asia.
Topics: Asia; Body Mass Index; Diet; Genetic Predisposition to Disease; Hepatitis B, Chronic; Humans; Incide | 2017 |
New trends on obesity and NAFLD in Asia.
Topics: Asia; Body Mass Index; Diet; Genetic Predisposition to Disease; Hepatitis B, Chronic; Humans; Incide | 2017 |
New trends on obesity and NAFLD in Asia.
Topics: Asia; Body Mass Index; Diet; Genetic Predisposition to Disease; Hepatitis B, Chronic; Humans; Incide | 2017 |
New trends on obesity and NAFLD in Asia.
Topics: Asia; Body Mass Index; Diet; Genetic Predisposition to Disease; Hepatitis B, Chronic; Humans; Incide | 2017 |
New trends on obesity and NAFLD in Asia.
Topics: Asia; Body Mass Index; Diet; Genetic Predisposition to Disease; Hepatitis B, Chronic; Humans; Incide | 2017 |
NAFLD-NASH: An Under-Recognized Epidemic.
Topics: Coronary Artery Disease; Epidemics; Female; Genetic Predisposition to Disease; Global Health; Hispan | 2018 |
Role of nutrition, gene polymorphism, and gut microbiota in non-alcoholic fatty liver disease.
Topics: Animals; Dietary Carbohydrates; Dietary Fats; Energy Intake; Gastrointestinal Microbiome; Humans; Li | 2017 |
Nonalcoholic Fatty Liver Disease and Metabolic Syndrome.
Topics: Dyslipidemias; Humans; Hyperglycemia; Hypertension; Lipase; Membrane Proteins; Metabolic Syndrome; N | 2018 |
Nonalcoholic Fatty Liver Disease/Nonalcoholic Steatohepatitis in Liver Transplantation.
Topics: Cardiovascular Diseases; Diabetes Complications; Humans; Kidney Diseases; Lipase; Liver Transplantat | 2018 |
The Genetics of Pediatric Nonalcoholic Fatty Liver Disease.
Topics: Acyltransferases; Adolescent; Alanine Transaminase; Apoptosis Regulatory Proteins; Basic Helix-Loop- | 2018 |
Risk Factors for the Development of Nonalcoholic Fatty Liver Disease/Nonalcoholic Steatohepatitis, Including Genetics.
Topics: Acyltransferases; Asian People; Black or African American; Diabetes Mellitus, Type 2; Female; Hispan | 2018 |
Disturbed Vitamin A Metabolism in Non-Alcoholic Fatty Liver Disease (NAFLD).
Topics: Adipose Tissue; Animals; Cell Transdifferentiation; Genetic Predisposition to Disease; Genetic Varia | 2017 |
The genetic backgrounds in nonalcoholic fatty liver disease.
Topics: Adaptor Proteins, Signal Transducing; Disease Progression; Genetic Background; Humans; Lipase; Membr | 2018 |
The relationship between obesity and the severity of non-alcoholic fatty liver disease: systematic review and meta-analysis.
Topics: Adult; Aged; Disease Progression; Genetic Predisposition to Disease; Humans; Lipase; Membrane Protei | 2018 |
Genetics of alcoholic liver disease and non-alcoholic steatohepatitis.
Topics: Acyltransferases; Disease Progression; Genetic Association Studies; Genetic Predisposition to Diseas | 2018 |
Recent research trends and updates on nonalcoholic fatty liver disease.
Topics: Chalcones; Cholesterol Ester Transfer Proteins; Clinical Trials as Topic; Enzyme Inhibitors; Humans; | 2019 |
Non-alcoholic fatty liver disease: causes, diagnosis, cardiometabolic consequences, and treatment strategies.
Topics: Antioxidants; Bariatric Surgery; Carcinoma, Hepatocellular; Cardiovascular Diseases; Diabetes Mellit | 2019 |
Non-alcoholic fatty liver disease: causes, diagnosis, cardiometabolic consequences, and treatment strategies.
Topics: Antioxidants; Bariatric Surgery; Carcinoma, Hepatocellular; Cardiovascular Diseases; Diabetes Mellit | 2019 |
Non-alcoholic fatty liver disease: causes, diagnosis, cardiometabolic consequences, and treatment strategies.
Topics: Antioxidants; Bariatric Surgery; Carcinoma, Hepatocellular; Cardiovascular Diseases; Diabetes Mellit | 2019 |
Non-alcoholic fatty liver disease: causes, diagnosis, cardiometabolic consequences, and treatment strategies.
Topics: Antioxidants; Bariatric Surgery; Carcinoma, Hepatocellular; Cardiovascular Diseases; Diabetes Mellit | 2019 |
Genetics of Nonalcoholic Fatty Liver Disease: A 2018 Update.
Topics: Apolipoproteins B; Disease Progression; Gene-Environment Interaction; Humans; Insulin Resistance; Li | 2018 |
Clinical-morphological parallels of the PNPLA3 gene polymorphism in patients with nonalcoholic fatty liver disease.
Topics: Humans; Lipase; Liver; Liver Cirrhosis; Liver Neoplasms; Membrane Proteins; Non-alcoholic Fatty Live | 2018 |
Association between PNPLA3 rs738409 polymorphism and nonalcoholic fatty liver disease (NAFLD) susceptibility and severity: A meta-analysis.
Topics: Age Factors; Alanine Transaminase; Alleles; Case-Control Studies; Female; Genetic Predisposition to | 2019 |
PNPLA3-I148M: a problem of plenty in non-alcoholic fatty liver disease.
Topics: Animals; Autophagy; Humans; Lipase; Lipid Droplets; Membrane Proteins; Mutation, Missense; Non-alcoh | 2019 |
Genome-Wide Association Study Identifies Loci for Liver Enzyme Concentrations in Mexican Americans: The GUARDIAN Consortium.
Topics: Adult; Alanine Transaminase; Aspartate Aminotransferases; Female; gamma-Glutamyltransferase; Genetic | 2019 |
Characterization of European ancestry nonalcoholic fatty liver disease-associated variants in individuals of African and Hispanic descent.
Topics: Adaptor Proteins, Signal Transducing; Adult; Aged; Black People; Chondroitin Sulfate Proteoglycans; | 2013 |
[Genetic predisposition related to non-alcoholic fatty liver disease].
Topics: Fatty Liver; Genetic Predisposition to Disease; Genome-Wide Association Study; Humans; Lipase; Membr | 2013 |
The genetics of NAFLD.
Topics: Disease Progression; Epigenomics; Fatty Liver; Genome-Wide Association Study; Humans; Lipase; Membra | 2013 |
PNPLA3-associated steatohepatitis: toward a gene-based classification of fatty liver disease.
Topics: Age Factors; Animals; Fatty Liver; Gene Frequency; Genetic Predisposition to Disease; Genetic Variat | 2013 |
PNPLA3 I148M polymorphism and progressive liver disease.
Topics: Carcinoma, Hepatocellular; Cholangitis, Sclerosing; Disease Progression; Fatty Liver; Fatty Liver, A | 2013 |
Obesity-associated nonalcoholic fatty liver disease.
Topics: Adult; Bariatric Surgery; Child; Fatty Liver; Female; Humans; Insulin Resistance; Lipase; Male; Memb | 2014 |
Host genetic variants in obesity-related nonalcoholic fatty liver disease.
Topics: Adipogenesis; Apolipoprotein C-III; Carrier Proteins; Fatty Liver; Genetic Association Studies; Hemo | 2014 |
Non-alcoholic fatty liver disease as a cause and a consequence of metabolic syndrome.
Topics: Diabetes Mellitus, Type 2; Fatty Liver; Female; Humans; Lipase; Male; Membrane Proteins; Metabolic S | 2014 |
Non-alcoholic fatty liver disease and type 2 diabetes mellitus: the liver disease of our age?
Topics: Adiposity; Animals; Diabetes Mellitus, Type 2; Diacylglycerol O-Acyltransferase; Diagnostic Imaging; | 2014 |
Role of metabolic lipases and lipolytic metabolites in the pathogenesis of NAFLD.
Topics: Animals; Disease Progression; Humans; Lipase; Lipolysis; Liver; Non-alcoholic Fatty Liver Disease; R | 2014 |
PNPLA3 I148M variant in nonalcoholic fatty liver disease: demographic and ethnic characteristics and the role of the variant in nonalcoholic fatty liver fibrosis.
Topics: Ethnicity; Female; Genetic Association Studies; Genetic Predisposition to Disease; Humans; Lipase; L | 2015 |
PNPLA3 polymorphisms (rs738409) and non-alcoholic fatty liver disease risk and related phenotypes: a meta-analysis.
Topics: Alanine Transaminase; Alleles; Asian People; Case-Control Studies; Databases, Bibliographic; Fibrosi | 2015 |
Practical approach to non-alcoholic fatty liver disease in patients with diabetes.
Topics: Biomarkers; Diabetes Mellitus, Type 2; Diet; Gastrointestinal Microbiome; Hepatitis; Humans; Hypogly | 2015 |
A Perspective on Metabolic Syndrome and Nonalcoholic Fatty Liver Disease.
Topics: Biomarkers; Diabetes Mellitus, Type 2; Genetic Predisposition to Disease; Genetic Variation; Humans; | 2015 |
Association between patatin-like phospholipase domain containing 3 gene (PNPLA3) polymorphisms and nonalcoholic fatty liver disease: a HuGE review and meta-analysis.
Topics: Case-Control Studies; Humans; Lipase; Membrane Proteins; Non-alcoholic Fatty Liver Disease; Polymorp | 2015 |
Autophagy and Lipid Droplets in the Liver.
Topics: Animals; Autophagy; Autophagy-Related Protein 7; Gene Deletion; Hepatocytes; Homeostasis; Humans; Li | 2015 |
Challenges and Management of Liver Cirrhosis: Practical Issues in the Therapy of Patients with Cirrhosis due to NAFLD and NASH.
Topics: Anticholesteremic Agents; Antioxidants; Bariatric Surgery; Carcinoma, Hepatocellular; Disease Progre | 2015 |
The Genetics of Nonalcoholic Fatty Liver Disease: Spotlight on PNPLA3 and TM6SF2.
Topics: Animals; Disease Progression; Genetic Association Studies; Genetic Markers; Genetic Predisposition t | 2015 |
Insights from Genome-Wide Association Analyses of Nonalcoholic Fatty Liver Disease.
Topics: Adaptor Proteins, Signal Transducing; Carcinoma, Hepatocellular; Genetic Predisposition to Disease; | 2015 |
Bidirectional Relationships and Disconnects between NAFLD and Features of the Metabolic Syndrome.
Topics: Animals; Female; Genetic Predisposition to Disease; Genetic Variation; Genotype; Humans; Insulin Res | 2016 |
The Prevalence and Pathobiology of Nonalcoholic Fatty Liver Disease in Patients of Different Races or Ethnicities.
Topics: Black or African American; Hispanic or Latino; Humans; Lipase; Membrane Proteins; Metabolic Syndrome | 2016 |
Diagnosis of non-alcoholic fatty liver disease (NAFLD).
Topics: Alanine Transaminase; Genotype; Humans; Lipase; Membrane Proteins; Metabolic Syndrome; Non-alcoholic | 2016 |
Definitions of Normal Liver Fat and the Association of Insulin Sensitivity with Acquired and Genetic NAFLD-A Systematic Review.
Topics: Humans; Insulin; Insulin Resistance; Lipase; Liver; Magnetic Resonance Imaging; Membrane Proteins; N | 2016 |
Pharmacogenomic and personalized approaches to tackle nonalcoholic fatty liver disease.
Topics: Female; Humans; Lipase; Male; Membrane Proteins; Non-alcoholic Fatty Liver Disease; Pharmacogenetics | 2016 |
Non-alcoholic fatty liver disease and risk of type 2 diabetes.
Topics: Biomarkers; Diabetes Mellitus, Type 2; Humans; Lipase; Membrane Proteins; Non-alcoholic Fatty Liver | 2016 |
Genetic factors that affect nonalcoholic fatty liver disease: A systematic clinical review.
Topics: Alpha-Ketoglutarate-Dependent Dioxygenase FTO; Genetic Predisposition to Disease; Heme Oxygenase-1; | 2016 |
Hepatocellular carcinoma in patients with non-alcoholic fatty liver disease.
Topics: Adiponectin; Carcinoma, Hepatocellular; Disease Progression; Humans; Immune System; Inflammation; Li | 2016 |
Genetic predisposition in nonalcoholic fatty liver disease.
Topics: Genetic Predisposition to Disease; Humans; Lipase; Liver; Membrane Proteins; Non-alcoholic Fatty Liv | 2017 |
Significance of genetic polymorphisms in patients with nonalcoholic fatty liver disease.
Topics: Genetic Predisposition to Disease; Humans; Lipase; Membrane Proteins; Non-alcoholic Fatty Liver Dise | 2017 |
Meta-analysis of the influence of I148M variant of patatin-like phospholipase domain containing 3 gene (PNPLA3) on the susceptibility and histological severity of nonalcoholic fatty liver disease.
Topics: Adult; Alanine Transaminase; Child; Fatty Liver; Female; Genetic Predisposition to Disease; Heterozy | 2011 |
Genome-wide association analysis identifies variants associated with nonalcoholic fatty liver disease that have distinct effects on metabolic traits.
Topics: Adaptor Proteins, Signal Transducing; Adult; Aged; Aged, 80 and over; Blood Glucose; Case-Control St | 2011 |
Genetics in liver disease: new concepts.
Topics: Autoimmune Diseases; Cholestasis; Fatty Liver; Genetic Predisposition to Disease; Genome-Wide Associ | 2011 |
Genetic determinants of susceptibility and severity in nonalcoholic fatty liver disease.
Topics: Animals; Cytokines; Disease Progression; Fatty Liver; Female; Genetic Predisposition to Disease; Gen | 2011 |
Liver triacylglycerol lipases.
Topics: Animals; Autophagy; Diabetes Mellitus, Type 2; Esterases; Fatty Liver; Hepatocytes; Humans; Lipase; | 2012 |
[Influence of non-alcoholic fatty liver disease on cardiovascular disease].
Topics: Apolipoprotein C-III; Atherosclerosis; Cardiovascular Diseases; Carotid Intima-Media Thickness; Chol | 2012 |
The genetic epidemiology of nonalcoholic fatty liver disease: toward a personalized medicine.
Topics: Epigenomics; Fatty Liver; Female; Genetic Loci; Genetic Predisposition to Disease; Genetic Variation | 2012 |
11 trials available for 1-anilino-8-naphthalenesulfonate and Non-alcoholic Fatty Liver Disease
| Article | Year |
|---|---|
Clinical Intervention to Reduce Dietary Sugar Does Not Affect Liver Fat in Latino Youth, Regardless of PNPLA3 Genotype: A Randomized Controlled Trial.
Topics: Adolescent; Child; Cross-Sectional Studies; Dietary Sugars; Genetic Predisposition to Disease; Genot | 2022 |
Four-Week Omega-3 Supplementation in Carriers of the Prosteatotic PNPLA3 p.I148M Genetic Variant: An Open-Label Study.
Topics: Adolescent; Adult; Aged; Amino Acid Substitution; Dietary Supplements; Elasticity Imaging Techniques | 2019 |
A Placebo-Controlled Trial of Subcutaneous Semaglutide in Nonalcoholic Steatohepatitis.
Topics: Adolescent; Adult; Aged; Amylases; Biopsy; Diabetes Mellitus, Type 2; Dose-Response Relationship, Dr | 2021 |
A Placebo-Controlled Trial of Subcutaneous Semaglutide in Nonalcoholic Steatohepatitis.
Topics: Adolescent; Adult; Aged; Amylases; Biopsy; Diabetes Mellitus, Type 2; Dose-Response Relationship, Dr | 2021 |
A Placebo-Controlled Trial of Subcutaneous Semaglutide in Nonalcoholic Steatohepatitis.
Topics: Adolescent; Adult; Aged; Amylases; Biopsy; Diabetes Mellitus, Type 2; Dose-Response Relationship, Dr | 2021 |
A Placebo-Controlled Trial of Subcutaneous Semaglutide in Nonalcoholic Steatohepatitis.
Topics: Adolescent; Adult; Aged; Amylases; Biopsy; Diabetes Mellitus, Type 2; Dose-Response Relationship, Dr | 2021 |
Impact of the Association Between PNPLA3 Genetic Variation and Dietary Intake on the Risk of Significant Fibrosis in Patients With NAFLD.
Topics: Adult; Biopsy; Diet Surveys; Female; Genotype; Humans; Lipase; Liver Cirrhosis; Male; Membrane Prote | 2021 |
Randomized Controlled Trial of a MUFA or Fiber-Rich Diet on Hepatic Fat in Prediabetes.
Topics: Adaptor Proteins, Signal Transducing; Aged; Chondroitin Sulfate Proteoglycans; Deuterium; Dietary Fa | 2017 |
Genome-wide scan revealed that polymorphisms in the PNPLA3, SAMM50, and PARVB genes are associated with development and progression of nonalcoholic fatty liver disease in Japan.
Topics: Actinin; Adult; Age Factors; Aged; Alanine Transaminase; Asian People; Aspartate Aminotransferases; | 2013 |
The I148M variant of PNPLA3 reduces the response to docosahexaenoic acid in children with non-alcoholic fatty liver disease.
Topics: Child; Child, Preschool; Docosahexaenoic Acids; Fatty Liver; Female; Humans; Lipase; Male; Membrane | 2013 |
Genetic variants in GCKR and PNPLA3 confer susceptibility to nonalcoholic fatty liver disease in obese individuals.
Topics: Adaptor Proteins, Signal Transducing; Adolescent; Alleles; Asian People; Body Mass Index; Child; Fat | 2014 |
Treating liver fat and serum triglyceride levels in NAFLD, effects of PNPLA3 and TM6SF2 genotypes: Results from the WELCOME trial.
Topics: Adult; Aged; Dietary Supplements; Docosahexaenoic Acids; Double-Blind Method; Drug Combinations; Eic | 2015 |
Effect of short-term carbohydrate overfeeding and long-term weight loss on liver fat in overweight humans.
Topics: Adult; Body Mass Index; Diet, Reducing; Dietary Carbohydrates; Dietary Sucrose; Fatty Liver; Female; | 2012 |
A common variant in the peroxisome proliferator-activated receptor-γ coactivator-1α gene is associated with nonalcoholic fatty liver disease in obese children.
Topics: Adolescent; Alleles; Body Mass Index; Child; Cohort Studies; Fatty Liver; Female; Genetic Associatio | 2013 |
291 other studies available for 1-anilino-8-naphthalenesulfonate and Non-alcoholic Fatty Liver Disease
| Article | Year |
|---|---|
Single nucleotide polymorphisms in PNPLA3, ADAR-1 and IFIH1 are associated with advanced liver fibrosis in patients co-infected with HIV-1//hepatitis C virus.
Topics: Acyltransferases; Adenosine Deaminase; Coinfection; Hepacivirus; Hepatitis C, Chronic; HIV Infection | 2021 |
Effects of PNPLA3, TM6SF2 and SAMM50 on the development and severity of non-alcoholic fatty liver disease in children.
Topics: Acyltransferases; Adolescent; Child; Genetic Predisposition to Disease; Genotype; Humans; Lipase; Li | 2022 |
Association of PNPLA3 I148M with Liver Disease Biomarkers in Latinos.
Topics: Biomarkers; Female; Genetic Predisposition to Disease; Hispanic or Latino; Humans; Lipase; Male; Mem | 2021 |
The Risk of Cirrhosis and Its Complications Based on PNPLA3 rs738409 G Allele Frequency.
Topics: Acyltransferases; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Gene Frequency; Genet | 2022 |
Correlations between PNPLA3 Gene Polymorphisms and NAFLD in Type 2 Diabetic Patients.
Topics: Carotid Intima-Media Thickness; Diabetes Mellitus, Type 2; Genetic Predisposition to Disease; Genoty | 2021 |
Protective association of Klotho rs495392 gene polymorphism against hepatic steatosis in non-alcoholic fatty liver disease patients.
Topics: Genetic Predisposition to Disease; Humans; Klotho Proteins; Lipase; Liver; Membrane Proteins; Non-al | 2022 |
PNPLA3 downregulation exacerbates the fibrotic response in human hepatic stellate cells.
Topics: Adult; Aged; Cells, Cultured; Down-Regulation; Female; Gene Expression Regulation; Hepatic Stellate | 2021 |
Body Mass Index and PNPLA3 Genetic Variant Modify the Association of Alcohol Consumption With Liver Fat Content.
Topics: Alcohol Drinking; Body Mass Index; Genetic Predisposition to Disease; Humans; Lipase; Liver; Non-alc | 2022 |
NAFLD-related gene polymorphisms and all-cause and cause-specific mortality in an Asian population: the Shanghai Changfeng Study.
Topics: Adult; Cardiovascular Diseases; Cause of Death; China; Genetic Predisposition to Disease; Genome-Wid | 2022 |
The influence of host genetics on liver microbiome composition in patients with NAFLD.
Topics: Genetic Predisposition to Disease; Genotype; Humans; Lipase; Liver; Membrane Proteins; Microbiota; N | 2022 |
PNPLA3 I148M Polymorphism Influences Renal Function in Children With Obesity and Prediabetes.
Topics: Child; Humans; Kidney; Lipase; Membrane Proteins; Non-alcoholic Fatty Liver Disease; Obesity; Predia | 2022 |
Interaction between Lifestyle Changes and PNPLA3 Genotype in NAFLD Patients during the COVID-19 Lockdown.
Topics: Communicable Disease Control; COVID-19; Genotype; Humans; Life Style; Lipase; Membrane Proteins; Non | 2022 |
The association between rs1260326 with the risk of NAFLD and the mediation effect of triglyceride on NAFLD in the elderly Chinese Han population.
Topics: Aged; Case-Control Studies; China; Genetic Predisposition to Disease; Genotype; Humans; Lipase; Memb | 2022 |
PNPLA3 rs738409 and risk of fibrosis in NAFLD: Exploring mediation pathways through intermediate histological features.
Topics: Fibrosis; Genetic Predisposition to Disease; Humans; Inflammation; Lipase; Liver; Membrane Proteins; | 2022 |
Should PNPLA3 polymorphism be performed in clinical practice in patients with NAFLD to predict the risk of disease progression?
Topics: Disease Progression; Genetic Predisposition to Disease; Genotype; Humans; Lipase; Non-alcoholic Fatt | 2022 |
Non-Alcoholic Fatty Liver Disease in Long-Term Type 2 Diabetes: Role of rs738409
Topics: Acyltransferases; Biomarkers; Diabetes Mellitus, Type 2; Fibroblast Growth Factors; Humans; Lipase; | 2022 |
A multiancestry genome-wide association study of unexplained chronic ALT elevation as a proxy for nonalcoholic fatty liver disease with histological and radiological validation.
Topics: Alanine Transaminase; Alpha-Ketoglutarate-Dependent Dioxygenase FTO; Genome-Wide Association Study; | 2022 |
Personalized medicine in nonalcoholic fatty liver disease.
Topics: Genetic Predisposition to Disease; Humans; Lipase; Liver; Non-alcoholic Fatty Liver Disease; Precisi | 2022 |
Low skeletal muscle mass is associated with more severe histological features of non-alcoholic fatty liver disease in male.
Topics: Creatinine; Genetic Predisposition to Disease; Humans; Lipase; Liver; Male; Membrane Proteins; Muscl | 2022 |
Hepatic patatin-like phospholipase domain-containing 3 levels are increased in I148M risk allele carriers and correlate with NAFLD in humans.
Topics: Acyltransferases; Alleles; Animals; Fibrosis; Humans; Inflammation; Lipase; Membrane Proteins; Non-a | 2022 |
Genetic variants associated with metabolic dysfunction-associated fatty liver disease in western China.
Topics: Genetic Predisposition to Disease; Genotype; Glucose; Humans; Lipase; Liver; Liver Diseases; Membran | 2022 |
Association of rs738409 Polymorphism in Adiponutrin Gene with Liver Steatosis and Atherosclerosis Risk Factors in Greek Children and Adolescents.
Topics: Acyltransferases; Adolescent; Atherosclerosis; Child; Genetic Predisposition to Disease; Genotype; G | 2022 |
Human hepatocyte PNPLA3-148M exacerbates rapid non-alcoholic fatty liver disease development in chimeric mice.
Topics: Acyltransferases; Animals; Hepatocytes; Humans; Lipase; Membrane Proteins; Mice; Non-alcoholic Fatty | 2022 |
Effect of common genetic variants on the risk of cirrhosis in non-alcoholic fatty liver disease during 20 years of follow-up.
Topics: Diabetes Mellitus, Type 2; Fibrosis; Follow-Up Studies; Humans; Lipase; Liver Cirrhosis; Membrane Pr | 2022 |
Profiling of cell-free DNA methylation and histone signatures in pediatric NAFLD: A pilot study.
Topics: Adolescent; Cell-Free Nucleic Acids; Child; DNA Methylation; Histones; Humans; Lipase; Membrane Prot | 2022 |
A machine-learning approach for nonalcoholic steatohepatitis susceptibility estimation.
Topics: Genetic Predisposition to Disease; Humans; Lipase; Machine Learning; Membrane Proteins; Non-alcoholi | 2022 |
Rhynchophylline relieves nonalcoholic fatty liver disease by activating lipase and increasing energy metabolism.
Topics: Animals; Diet, High-Fat; Lipase; Lipid Metabolism; Liver; Mice; Mice, Inbred C57BL; Non-alcoholic Fa | 2023 |
Loss of KDM6B epigenetically confers resistance to lipotoxicity in nonalcoholic fatty liver disease-related HCC.
Topics: Animals; Carcinoma, Hepatocellular; Cell Cycle Proteins; Humans; Jumonji Domain-Containing Histone D | 2023 |
Association Between PNPLA3 rs738409 C>G Variant and Liver-Related Outcomes in Patients With Nonalcoholic Fatty Liver Disease.
Topics: Carcinoma, Hepatocellular; Genetic Predisposition to Disease; Genotype; Humans; Lipase; Liver Neopla | 2020 |
PNPLA3 rs738409 is associated with renal glomerular and tubular injury in NAFLD patients with persistently normal ALT levels.
Topics: Adult; Alanine Transaminase; Alleles; Case-Control Studies; Female; Genetic Predisposition to Diseas | 2020 |
Association Between a Polymorphism in MBOAT7 and Chronic Kidney Disease in Patients With Biopsy-Confirmed Nonalcoholic Fatty Liver Disease.
Topics: Acyltransferases; Biopsy; Genetic Predisposition to Disease; Humans; Lipase; Liver; Membrane Protein | 2020 |
Effect of PNPLA3 polymorphism on diagnostic performance of various noninvasive markers for diagnosing and staging nonalcoholic fatty liver disease.
Topics: Adult; Diagnostic Techniques, Digestive System; Female; Genotype; Humans; Lipase; Male; Membrane Pro | 2020 |
Patatin-Like Phospholipase Domain-Containing Protein 3 I148M and Liver Fat and Fibrosis Scores Predict Liver Disease Mortality in the U.S. Population.
Topics: Adipose Tissue; Adult; Female; Humans; Lipase; Liver; Liver Cirrhosis; Male; Membrane Proteins; Midd | 2020 |
Factors influencing subclinical atherosclerosis in patients with biopsy-proven nonalcoholic fatty liver disease.
Topics: Adolescent; Adult; Age Factors; Aged; Aged, 80 and over; Ankle Brachial Index; Atherosclerosis; Fema | 2019 |
PNPLA3 I148M Polymorphism in Patients with Nonalcoholic Fatty Liver Disease, Obesity and Prediabetes.
Topics: Adult; Aged; Anthropometry; Female; Genetic Predisposition to Disease; Genotype; Humans; Lipase; Mal | 2019 |
FIB-4 Index and Diabetes Mellitus Are Associated with Chronic Kidney Disease in Japanese Patients with Non-Alcoholic Fatty Liver Disease.
Topics: Adult; Aged; Aged, 80 and over; Diabetes Mellitus, Type 2; Female; Glomerular Filtration Rate; Human | 2019 |
Risk factors for histological progression of non-alcoholic steatohepatitis analyzed from repeated biopsy cases.
Topics: Adult; Aged; Aged, 80 and over; Alanine Transaminase; Alleles; Biomarkers; Biopsy; Disease Progressi | 2020 |
Transmembrane 6 superfamily member 2 167K allele improves renal function in children with obesity.
Topics: Adolescent; Alleles; Body Mass Index; Child; Female; Genetic Predisposition to Disease; Genotype; Gl | 2020 |
Association of metabolic syndrome and patatin-like phospholipase 3 - rs738409 gene variant in non-alcoholic fatty liver disease among a Chennai-based south Indian population.
Topics: Adult; Aged; Alleles; Biomarkers; Case-Control Studies; Disease Susceptibility; Female; Genetic Pred | 2020 |
The endothelial function biomarker soluble E-selectin is associated with nonalcoholic fatty liver disease.
Topics: Adaptor Proteins, Signal Transducing; Animals; Biomarkers; Cadherins; Lipase; Liver; Mice; Mice, Inb | 2020 |
Liver transcriptomics highlights interleukin-32 as novel NAFLD-related cytokine and candidate biomarker.
Topics: Adult; Biomarkers; Disease Progression; Drug Discovery; Female; Gene Expression Profiling; Genetic P | 2020 |
PNPLA3 polymorphism influences the association between high-normal TSH level and NASH in euthyroid adults with biopsy-proven NAFLD.
Topics: Adult; Alleles; Female; Genetic Predisposition to Disease; Humans; Lipase; Liver; Logistic Models; M | 2020 |
Metabolic regulation of hepatic PNPLA3 expression and severity of liver fibrosis in patients with NASH.
Topics: Humans; Lipase; Liver; Liver Cirrhosis; Membrane Proteins; Non-alcoholic Fatty Liver Disease | 2020 |
Development and Validation of a Scoring System, Based on Genetic and Clinical Factors, to Determine Risk of Steatohepatitis in Asian Patients with Nonalcoholic Fatty Liver Disease.
Topics: Genotype; Humans; Insulin Resistance; Lipase; Liver; Membrane Proteins; Non-alcoholic Fatty Liver Di | 2020 |
Independent and joint correlation of PNPLA3 I148M and TM6SF2 E167K variants with the risk of coronary heart disease in patients with non-alcoholic fatty liver disease.
Topics: Alleles; Coronary Disease; Female; Gene Frequency; Genetic Predisposition to Disease; Genotype; Huma | 2020 |
PNPLA3 I148M gene variant and chronic kidney disease in type 2 diabetic patients with NAFLD: Clinical and experimental findings.
Topics: Diabetes Mellitus, Type 2; Genetic Predisposition to Disease; Humans; Lipase; Membrane Proteins; Non | 2020 |
Glucagon stimulates gluconeogenesis by INSP3R1-mediated hepatic lipolysis.
Topics: Acetyl Coenzyme A; Adipose Tissue; Animals; Diabetes Mellitus, Type 2; Enzyme Activation; Glucagon; | 2020 |
A common variant in PNPLA3 is associated with age at diagnosis of NAFLD in patients from a multi-ethnic biobank.
Topics: Adolescent; Adult; Age Factors; Aged; Aged, 80 and over; Alleles; Biological Specimen Banks; Case-Co | 2020 |
Causal relationships between NAFLD, T2D and obesity have implications for disease subphenotyping.
Topics: Animals; Causality; Diabetes Mellitus, Type 2; Europe; Founder Effect; Genome-Wide Association Study | 2020 |
Combined Effect of PNPLA3, TM6SF2, and HSD17B13 Variants on Risk of Cirrhosis and Hepatocellular Carcinoma in the General Population.
Topics: 17-Hydroxysteroid Dehydrogenases; Alanine Transaminase; Carcinoma, Hepatocellular; Denmark; Female; | 2020 |
PNPLA3 gene polymorphism and overall and cardiovascular mortality in the United States.
Topics: Adult; Alleles; Cardiovascular Diseases; Comorbidity; Female; Follow-Up Studies; Genetic Association | 2020 |
The PNPLA3 rs738409 GG genotype is associated with poorer prognosis in 239 patients with autoimmune hepatitis.
Topics: Adolescent; Adult; Aged; Child; Child, Preschool; Disease Progression; Female; Follow-Up Studies; Ge | 2020 |
The effect of PNPLA3 polymorphism as gain in function mutation in the pathogenesis of non-alcoholic fatty liver disease.
Topics: Carcinoma, Hepatocellular; Deception; Humans; Lipase; Liver Neoplasms; Membrane Proteins; Metabolic | 2020 |
Attenuated effect of PNPLA3 on hepatic fibrosis by HSD17B13 in Japanese patients with non-alcoholic fatty liver disease.
Topics: Humans; Japan; Lipase; Liver; Liver Cirrhosis; Liver Neoplasms; Membrane Proteins; Non-alcoholic Fat | 2020 |
PNPLA3 Gene Polymorphism and Liver- and Extrahepatic Cancer-Related Mortality in the United States.
Topics: Carcinoma, Hepatocellular; Female; Genetic Predisposition to Disease; Humans; Lipase; Liver; Liver N | 2021 |
The PNPLA3-I148M variant increases polyunsaturated triglycerides in human adipose tissue.
Topics: Adipose Tissue; Genetic Predisposition to Disease; Humans; Lipase; Membrane Proteins; Non-alcoholic | 2020 |
Genetic Susceptibility to Chronic Liver Disease in Individuals from Pakistan.
Topics: 17-Hydroxysteroid Dehydrogenases; Acyltransferases; Adaptor Proteins, Signal Transducing; Adult; Chr | 2020 |
How do genetic variants affect our interpretation of non-invasive tests for non-alcoholic fatty liver disease?
Topics: Adaptor Proteins, Signal Transducing; Biomarkers; Diagnostic Techniques, Digestive System; Humans; K | 2020 |
Effect of Gut Microbiota and PNPLA3 rs738409 Variant on Nonalcoholic Fatty Liver Disease (NAFLD) in Obese Youth.
Topics: Adolescent; Child; Cross-Sectional Studies; DNA, Bacterial; Feces; Female; Gastrointestinal Microbio | 2020 |
Effect of Gut Microbiota and PNPLA3 rs738409 Variant on Nonalcoholic Fatty Liver Disease (NAFLD) in Obese Youth.
Topics: Adolescent; Child; Cross-Sectional Studies; DNA, Bacterial; Feces; Female; Gastrointestinal Microbio | 2020 |
Effect of Gut Microbiota and PNPLA3 rs738409 Variant on Nonalcoholic Fatty Liver Disease (NAFLD) in Obese Youth.
Topics: Adolescent; Child; Cross-Sectional Studies; DNA, Bacterial; Feces; Female; Gastrointestinal Microbio | 2020 |
Effect of Gut Microbiota and PNPLA3 rs738409 Variant on Nonalcoholic Fatty Liver Disease (NAFLD) in Obese Youth.
Topics: Adolescent; Child; Cross-Sectional Studies; DNA, Bacterial; Feces; Female; Gastrointestinal Microbio | 2020 |
Editorial: PNPLA3 genotype and liver diseases-more than non-alcoholic fatty liver disease. Authors' reply.
Topics: Genotype; Hepatitis, Autoimmune; Humans; Lipase; Non-alcoholic Fatty Liver Disease; Prognosis | 2020 |
Editorial: PNPLA3 genotype and liver diseases-more than non-alcoholic fatty liver disease.
Topics: Genotype; Hepatitis, Autoimmune; Humans; Lipase; Non-alcoholic Fatty Liver Disease; Prognosis | 2020 |
Association between PNPLA3 rs738409 G variant and MRI cerebrovascular disease biomarkers.
Topics: Aged; Biomarkers; Cross-Sectional Studies; Female; Genetic Predisposition to Disease; Humans; Lipase | 2020 |
PNPLA3 gene polymorphism is associated with liver steatosis in children with Down syndrome.
Topics: Adiponectin; Adolescent; Age Factors; Biomarkers; Blood Glucose; Child; Child, Preschool; Down Syndr | 2020 |
Validating a non-invasive, ALT-based non-alcoholic fatty liver phenotype in the million veteran program.
Topics: 17-Hydroxysteroid Dehydrogenases; Abdomen; Adaptor Proteins, Signal Transducing; Aged; Alanine Trans | 2020 |
PNPLA3 I148M is involved in the variability in anti-NAFLD response to exenatide.
Topics: Diabetes Mellitus, Type 2; Exenatide; Genetic Predisposition to Disease; Genotype; Hep G2 Cells; Hum | 2020 |
Interaction Between Alcohol Consumption and PNPLA3 Variant in the Prevalence of Hepatic Steatosis in the US Population.
Topics: Adult; Alcohol Drinking; Cross-Sectional Studies; Genetic Predisposition to Disease; Genotype; Human | 2021 |
PNPLA3 rs738409 C>G Variant Predicts Fibrosis Progression by Noninvasive Tools in Nonalcoholic Fatty Liver Disease.
Topics: Fibrosis; Genetic Predisposition to Disease; Humans; Lipase; Liver; Liver Cirrhosis; Membrane Protei | 2021 |
Validating candidate biomarkers for different stages of non-alcoholic fatty liver disease.
Topics: Adult; Biomarkers; Case-Control Studies; Disease Progression; Enzyme-Linked Immunosorbent Assay; Fem | 2020 |
Role of Patatin-Like Phospholipase Domain-Containing 3 Gene for Hepatic Lipid Content and Insulin Resistance in Diabetes.
Topics: Adult; Aged; Alleles; Case-Control Studies; Cross-Sectional Studies; Diabetes Mellitus, Type 2; Fema | 2020 |
Pediatric non-alcoholic fatty liver disease and kidney function: Effect of
Topics: Adolescent; Adult; Alanine Transaminase; Child; Genetic Predisposition to Disease; Humans; Kidney; L | 2020 |
Identification of a Metabolic, Transcriptomic, and Molecular Signature of Patatin-Like Phospholipase Domain Containing 3-Mediated Acceleration of Steatohepatitis.
Topics: Animals; Diet, High-Fat; Diet, Western; Disease Models, Animal; Disease Progression; Gene Expression | 2021 |
Effects of TM6SF2 E167K on hepatic lipid and very low-density lipoprotein metabolism in humans.
Topics: Apolipoprotein B-100; Female; Genetic Predisposition to Disease; Humans; Lipase; Lipid Metabolism; L | 2020 |
Association between positivity of serum autoantibodies and liver disease severity in patients with biopsy-proven NAFLD.
Topics: Adult; Autoantibodies; Biomarkers; Biopsy; Cross-Sectional Studies; Female; Humans; Lipase; Liver; L | 2021 |
POCU1b, the n-Butanol Soluble Fraction of Polygoni Cuspidati Rhizoma et Radix, Attenuates Obesity, Non-Alcoholic Fatty Liver, and Insulin Resistance via Inhibitions of Pancreatic Lipase, cAMP-Dependent PDE Activity, AMPK Activation, and SOCS-3 Suppression
Topics: 1-Butanol; AMP-Activated Protein Kinases; Animals; Fallopia japonica; Insulin Resistance; Lipase; Ma | 2020 |
Development and course of diabetes according to genetic factors and diabetes treatment among patients with nonalcoholic fatty liver disease.
Topics: Diabetes Mellitus, Type 2; Genetic Predisposition to Disease; Humans; Lipase; Male; Membrane Protein | 2021 |
The Health Impact of MAFLD, a Novel Disease Cluster of NAFLD, Is Amplified by the Integrated Effect of Fatty Liver Disease-Related Genetic Variants.
Topics: Disease Hotspot; Humans; Lipase; Membrane Proteins; Non-alcoholic Fatty Liver Disease; Polymorphism, | 2022 |
Palmitate induces fat accumulation via repressing FoxO1-mediated ATGL-dependent lipolysis in HepG2 hepatocytes.
Topics: 1-Acylglycerol-3-Phosphate O-Acyltransferase; Cell Cycle Proteins; Forkhead Box Protein O1; Hep G2 C | 2021 |
Discordant hepatic fatty acid oxidation and triglyceride hydrolysis leads to liver disease.
Topics: Animals; Carnitine O-Palmitoyltransferase; Disease Progression; Fatty Acids; Female; Hydrolysis; Lip | 2021 |
Greater liver PNPLA3 protein abundance in vivo and in vitro supports lower triglyceride accumulation in dairy cows.
Topics: Animals; Cattle; Cells, Cultured; Female; Gene Knockdown Techniques; Hepatocytes; Ketosis; Lipase; L | 2021 |
Mitochondrial haplogroup G is associated with nonalcoholic fatty liver disease, while haplogroup A mitigates the effects of PNPLA3.
Topics: Asian People; DNA, Mitochondrial; Genetic Association Studies; Genetic Predisposition to Disease; Ge | 2021 |
Emerging Metabolic and Transcriptomic Signature of PNPLA3-Associated NASH.
Topics: Animals; Disease Models, Animal; Humans; Lipase; Membrane Proteins; Metabolome; Mice; Non-alcoholic | 2021 |
Variants in PCSK7, PNPLA3 and TM6SF2 are risk factors for the development of cirrhosis in hereditary haemochromatosis.
Topics: Europe; Genotype; Hemochromatosis; Humans; Lipase; Liver Cirrhosis; Membrane Proteins; Non-alcoholic | 2021 |
The role of PNPLA3 and TM6SF2 polymorphisms on liver fibrosis and metabolic abnormalities in Brazilian patients with chronic hepatitis C.
Topics: Aged; Brazil; Cross-Sectional Studies; Genetic Predisposition to Disease; Genotype; Hepatitis C, Chr | 2021 |
Individualized Polygenic Risk Score Identifies NASH in the Eastern Asia Region: A Derivation and Validation Study.
Topics: 17-Hydroxysteroid Dehydrogenases; Adult; Biopsy; China; Cross-Sectional Studies; Female; Genetic Pre | 2021 |
Combined analysis of gut microbiota, diet and PNPLA3 polymorphism in biopsy-proven non-alcoholic fatty liver disease.
Topics: Aged; Biopsy; Cross-Sectional Studies; Diet; Gastrointestinal Microbiome; Humans; Lipase; Liver; Mem | 2021 |
A PNPLA3 Polymorphism Confers Lower Susceptibility to Incident Diabetes Mellitus in Subjects With Nonalcoholic Fatty Liver Disease.
Topics: Acyltransferases; Diabetes Mellitus; Genetic Predisposition to Disease; Genotype; Humans; Lipase; Li | 2022 |
Integrated Action of Autophagy and Adipose Tissue Triglyceride Lipase Ameliorates Diet-Induced Hepatic Steatosis in Liver-Specific PLIN2 Knockout Mice.
Topics: Adipose Tissue; Animals; Autophagy; Diet; Lipase; Lipid Metabolism; Liver; Male; Mice; Mice, Inbred | 2021 |
Attenuating Effects of Dieckol on High-Fat Diet-Induced Nonalcoholic Fatty Liver Disease by Decreasing the NLRP3 Inflammasome and Pyroptosis.
Topics: Animals; Benzofurans; Carnitine O-Palmitoyltransferase; Diet, High-Fat; Gene Expression; HMGB1 Prote | 2021 |
P2Y2R Deficiency Ameliorates Hepatic Steatosis by Reducing Lipogenesis and Enhancing Fatty Acid β-Oxidation through AMPK and PGC-1α Induction in High-Fat Diet-Fed Mice.
Topics: Acetyl-CoA Carboxylase; Alanine Transaminase; AMP-Activated Protein Kinases; Animals; Aspartate Amin | 2021 |
Combined effects of PNPLA3, TM6SF2 and HSD17B13 variants on severity of biopsy-proven non-alcoholic fatty liver disease.
Topics: 17-Hydroxysteroid Dehydrogenases; Biopsy; Genetic Predisposition to Disease; Genotype; Humans; Lipas | 2021 |
Perilipin 5 links mitochondrial uncoupled respiration in brown fat to healthy white fat remodeling and systemic glucose tolerance.
Topics: Adipose Tissue, Brown; Adipose Tissue, White; Adrenergic beta-3 Receptor Agonists; Animals; Cold Tem | 2021 |
The influence of RS738409 I148M polymorphism of patatin-like phospholipase domain containing 3 gene on the susceptibility of non-alcoholic fatty liver disease.
Topics: Adult; Blood Glucose; Body Mass Index; Case-Control Studies; Female; Gene Frequency; Genetic Predisp | 2021 |
Plasma and stool metabolomics to identify microbiota derived-biomarkers of metabolic dysfunction-associated fatty liver disease: effect of PNPLA3 genotype.
Topics: Biomarkers; Genotype; Humans; Lipase; Membrane Proteins; Metabolomics; Microbiota; Non-alcoholic Fat | 2021 |
Natural history of NASH.
Topics: Humans; Lipase; Liver Cirrhosis; Membrane Proteins; Non-alcoholic Fatty Liver Disease | 2021 |
Bile acids induced hepatic lipid accumulation in mice by inhibiting mRNA expression of patatin-like phospholipase domain containing 3 and microsomal triglyceride transfer protein.
Topics: Acyl-CoA Oxidase; Animals; Bile Acids and Salts; Carrier Proteins; Cholesterol; Diet; Hep G2 Cells; | 2021 |
The Propensity of the Human Liver to Form Large Lipid Droplets Is Associated with PNPLA3 Polymorphism, Reduced INSIG1 and NPC1L1 Expression and Increased Fibrogenetic Capacity.
Topics: Adult; Aged; Female; Gene Expression Regulation; Hepacivirus; Hepatocytes; Humans; Intracellular Sig | 2021 |
A genome-first approach to mortality and metabolic phenotypes in
Topics: Heterozygote; Homozygote; Humans; Lipase; Membrane Proteins; Mitochondrial Proteins; Non-alcoholic F | 2021 |
Assessing Interactions between
Topics: Adult; Cross-Sectional Studies; Diet; Genetic Predisposition to Disease; Genotype; Humans; Lipase; L | 2021 |
Modeling PNPLA3-Associated NAFLD Using Human-Induced Pluripotent Stem Cells.
Topics: Cell Differentiation; Cell Line; CRISPR-Cas Systems; Ethanol; Gene Knockout Techniques; Genetic Pred | 2021 |
Identification and Optimization of a Minor Allele-Specific siRNA to Prevent PNPLA3 I148M-Driven Nonalcoholic Fatty Liver Disease.
Topics: Alleles; Animals; Genome-Wide Association Study; Lipase; Liver; Membrane Proteins; Mice; Non-alcohol | 2021 |
PPARGC1A rs8192678 G>A polymorphism affects the severity of hepatic histological features and nonalcoholic steatohepatitis in patients with nonalcoholic fatty liver disease.
Topics: Genetic Predisposition to Disease; Humans; Lipase; Liver; Membrane Proteins; Non-alcoholic Fatty Liv | 2021 |
CD8
Topics: Amyloid beta-Protein Precursor; Animals; Animals, Genetically Modified; Blood Glucose; CD8-Positive | 2021 |
To Be or Not to Be: The Quest for Patatin-Like Phospholipase Domain Containing 3 p.I148M Function.
Topics: Humans; Lipase; Non-alcoholic Fatty Liver Disease; Phospholipases | 2021 |
Hepatocyte-specific deletion of adipose triglyceride lipase (adipose triglyceride lipase/patatin-like phospholipase domain containing 2) ameliorates dietary induced steatohepatitis in mice.
Topics: Adult; Animals; Diet, Carbohydrate Loading; Diet, High-Fat; Disease Models, Animal; Fatty Acids, Non | 2022 |
Adiposity amplifies the genetic risk of fatty liver disease conferred by multiple loci.
Topics: Adaptor Proteins, Signal Transducing; Adiposity; Alanine Transaminase; Cohort Studies; Genetic Predi | 2017 |
Polymorphism of receptor-type tyrosine-protein phosphatase delta gene in the development of non-alcoholic fatty liver disease.
Topics: Adult; Aged; Aged, 80 and over; Asian People; DNA Repair Enzymes; Exodeoxyribonucleases; Female; Gen | 2018 |
Ultra-high-field magnetic resonance spectroscopy in non-alcoholic fatty liver disease: Novel mechanistic and diagnostic insights of energy metabolism in non-alcoholic steatohepatitis and advanced fibrosis.
Topics: Adenosine Triphosphate; Adult; Biomarkers; Biopsy; Body Mass Index; Energy Metabolism; Fatty Acids; | 2017 |
Incidence and risk factors for non-alcoholic fatty liver disease: A 7-year follow-up study among urban, adult Sri Lankans.
Topics: Adult; Asian People; Diabetes Complications; Female; Follow-Up Studies; Genetic Association Studies; | 2017 |
Low Birthweight Increases the Likelihood of Severe Steatosis in Pediatric Non-Alcoholic Fatty Liver Disease.
Topics: Adolescent; Birth Weight; Child; Female; Genetic Predisposition to Disease; Genotype; Humans; Infant | 2017 |
New Discriminant Method for Identifying the Aggressive Disease Phenotype of Non-alcoholic Fatty Liver Disease.
Topics: Adult; Age Factors; Aged; Biopsy; Body Mass Index; Disease Progression; Female; Fibrosis; Genotype; | 2017 |
Combination of PNPLA3 and TLL1 polymorphism can predict advanced fibrosis in Japanese patients with nonalcoholic fatty liver disease.
Topics: Adolescent; Adult; Aged; Aged, 80 and over; Aspartate Aminotransferases; Body Mass Index; Cohort Stu | 2018 |
Identification of deleterious rare variants in MTTP, PNPLA3, and TM6SF2 in Japanese males and association studies with NAFLD.
Topics: Alleles; Asian People; Base Sequence; Carrier Proteins; Exons; Gene Expression; Gene Frequency; Gene | 2017 |
Association of single nucleotide polymorphism at PNPLA3 with fatty liver, steatohepatitis, and cirrhosis of liver.
Topics: Adult; Aged; Female; Genetic Association Studies; Genotyping Techniques; Humans; Lipase; Liver Cirrh | 2017 |
PNPLA3 variant and portal/periportal histological pattern in patients with biopsy-proven non-alcoholic fatty liver disease: a possible role for oxidative stress.
Topics: Biopsy; Female; Genetic Predisposition to Disease; Humans; Lipase; Liver; Macrophages; Male; Membran | 2017 |
Disease progression: Divergent paths.
Topics: Age Factors; Body Mass Index; Disease Progression; Epigenesis, Genetic; Genetic Predisposition to Di | 2017 |
Additive effects of PNPLA3 and TM6SF2 on the histological severity of non-alcoholic fatty liver disease.
Topics: Adipose Tissue; Cohort Studies; Fibrosis; Genetic Association Studies; Genetic Variation; Homeostasi | 2018 |
Genetic Polymorphisms of PNPLA3 and SAMM50 Are Associated with Nonalcoholic Fatty Liver Disease in a Korean Population.
Topics: Age Factors; Alanine Transaminase; Body Mass Index; Female; Genetic Predisposition to Disease; Genom | 2018 |
Causal relationship of hepatic fat with liver damage and insulin resistance in nonalcoholic fatty liver.
Topics: Acyltransferases; Adaptor Proteins, Signal Transducing; Adipose Tissue; Adult; Chronic Disease; Diab | 2018 |
Genetic variants in COL13A1, ADIPOQ and SAMM50, in addition to the PNPLA3 gene, confer susceptibility to elevated transaminase levels in an admixed Mexican population.
Topics: Adiponectin; Adult; Aged; Alanine Transaminase; Aspartate Aminotransferases; Case-Control Studies; C | 2018 |
Genetic determinants of hepatic steatosis and serum cytokeratin-18 fragment levels in Taiwanese children.
Topics: Acyltransferases; Adaptor Proteins, Signal Transducing; Adolescent; Child; Female; Genotype; Humans; | 2018 |
PNPLA3: A Determinant of Response to Low-Fructose Diet in Nonalcoholic Fatty Liver Disease.
Topics: Diet; Fructose; Humans; Lipase; Liver; Non-alcoholic Fatty Liver Disease | 2018 |
Natural Extracts Abolished Lipid Accumulation in Cells Harbouring non-favourable PNPLA3 genotype.
Topics: Acetyl-CoA C-Acetyltransferase; Agaricales; Cell Line, Tumor; Cynara scolymus; Flowers; Genotype; He | 2018 |
More Evidence for the Genetic Susceptibility of Mexican Population to Nonalcoholic Fatty Liver Disease through PNPLA3.
Topics: Adult; Case-Control Studies; Female; Gene Frequency; Genetic Association Studies; Genetic Predisposi | 2018 |
Alpha-syntrophin null mice are protected from non-alcoholic steatohepatitis in the methionine-choline-deficient diet model but not the atherogenic diet model.
Topics: Adipocytes; Adiponectin; Adiposity; Animals; Body Weight; Calcium-Binding Proteins; Cell Size; Choli | 2018 |
Replacement of soybean oil by fish oil increases cytosolic lipases activities in liver and adipose tissue from rats fed a high-carbohydrate diets.
Topics: Adipocytes; Adipose Tissue; Animal Feed; Animals; Cytosol; Dietary Carbohydrates; Disease Models, An | 2018 |
Evaluation of Polygenic Determinants of Non-Alcoholic Fatty Liver Disease (NAFLD) By a Candidate Genes Resequencing Strategy.
Topics: Adaptor Proteins, Signal Transducing; Alleles; Chondroitin Sulfate Proteoglycans; Female; Genetic As | 2018 |
Analysis of genotyping for predicting liver injury marker, procollagen III in persons at risk of non-alcoholic fatty liver disease.
Topics: Adaptor Proteins, Signal Transducing; Adult; Aged; Alleles; Cross-Sectional Studies; Diabetes Mellit | 2018 |
Prevalence and severity of nonalcoholic fatty liver disease by transient elastography: Genetic and metabolic risk factors in a general population.
Topics: Adult; Aged; Diabetes Mellitus; Elasticity Imaging Techniques; Female; Humans; Italy; Lipase; Liver; | 2018 |
A novel index including SNPs for the screening of nonalcoholic fatty liver disease among elder Chinese: A population-based study.
Topics: Adaptor Proteins, Signal Transducing; Aged; Apolipoprotein C-III; Asian People; ATP Binding Cassette | 2018 |
The Membrane-bound O-Acyltransferase7 rs641738 Variant in Pediatric Nonalcoholic Fatty Liver Disease.
Topics: Acyltransferases; Adolescent; Alanine Transaminase; Alleles; Child; Female; Genotype; Humans; Lipase | 2018 |
NAFLD risk alleles in PNPLA3, TM6SF2, GCKR and LYPLAL1 show divergent metabolic effects.
Topics: Adaptor Proteins, Signal Transducing; Adult; Alleles; Female; Genetic Predisposition to Disease; Gen | 2018 |
Liver fat content, non-alcoholic fatty liver disease, and risk of ischaemic heart disease.
Topics: Europe; Genotype; Humans; Lipase; Membrane Proteins; Myocardial Ischemia; Non-alcoholic Fatty Liver | 2018 |
Combining Genetic Variants to Improve Risk Prediction for NAFLD and Its Progression to Cirrhosis: A Proof of Concept Study.
Topics: Adult; Aged; Case-Control Studies; Disease Progression; Gene Frequency; Genetic Loci; Genotype; Huma | 2018 |
Circulating Phospholipid Patterns in NAFLD Patients Associated with a Combination of Metabolic Risk Factors.
Topics: Adult; Biomarkers; Case-Control Studies; Chromatography, High Pressure Liquid; Comorbidity; Elastici | 2018 |
Role of the PNPLA3 polymorphism rs738409 on silymarin + vitamin E response in subjects with non-alcoholic fatty liver disease.
Topics: Antioxidants; Drug Combinations; Female; Humans; Lipase; Male; Membrane Proteins; Middle Aged; Non-a | 2018 |
Establishment and characterization of an iPSC line from a 35 years old high grade patient with nonalcoholic fatty liver disease (30-40% steatosis) with homozygous wildtype PNPLA3 genotype.
Topics: Adult; Genotype; Homozygote; Humans; Induced Pluripotent Stem Cells; Lipase; Male; Membrane Proteins | 2018 |
Establishment and characterization of an iPSC line from a 58 years old high grade patient with nonalcoholic fatty liver disease (70% steatosis) with homozygous wildtype PNPLA3 genotype.
Topics: Female; Genotype; Homozygote; Humans; Induced Pluripotent Stem Cells; Lipase; Membrane Proteins; Mid | 2018 |
Study of Family Clustering and PNPLA3 Gene Polymorphism in Pediatric Non Alcoholic Fatty Liver Disease.
Topics: Adolescent; Child; Cross-Sectional Studies; Female; Genetic Markers; Genetic Predisposition to Disea | 2018 |
PNPLA3 variant M148 causes resistance to starvation-mediated lipid droplet autophagy in human hepatocytes.
Topics: Autophagosomes; Autophagy; Biopsy; Cathepsin B; Cohort Studies; Genetic Variation; Genotype; Hep G2 | 2019 |
Relationship between non-alcoholic steatohepatitis, PNPLA3 I148M genotype and bone mineral density in adolescents.
Topics: Absorptiometry, Photon; Adolescent; Alleles; Bone and Bones; Bone Density; Case-Control Studies; Chi | 2018 |
A polymorphism in the Irisin-encoding gene (FNDC5) associates with hepatic steatosis by differential miRNA binding to the 3'UTR.
Topics: 3' Untranslated Regions; Australia; Biopsy; Female; Fibronectins; Gene Expression Profiling; Humans; | 2019 |
Genetic determinants of steatosis and fibrosis progression in paediatric non-alcoholic fatty liver disease.
Topics: Adaptor Proteins, Signal Transducing; Adolescent; Age Factors; Case-Control Studies; Child; Disease | 2019 |
Promoting genetics in non-alcoholic fatty liver disease: Combined risk score through polymorphisms and clinical variables.
Topics: Disease Progression; Genetic Predisposition to Disease; Humans; Lipase; Liver; Membrane Proteins; No | 2018 |
Characteristics of non-alcoholic steatohepatitis among lean patients in Japan: Not uncommon and not always benign.
Topics: Adiposity; Adult; Body Mass Index; Comorbidity; Cross-Sectional Studies; Female; Humans; Insulin Res | 2019 |
[ANTHROPOMETRIC CHARACTERISTICS AND PARAMETERS OF LIPID-CARBOHYDRATE METABOLISM IN PATIENTS WITH NONALCOHOLIC FATTY LIVER DISEASE AND HYPERTENSION DEPENDING ON THE DEGREE OF HEPATIC STEATOSIS].
Topics: Blood Glucose; Body Weights and Measures; Carbohydrate Metabolism; Case-Control Studies; Female; Hum | 2018 |
The PNPLA3 rs738409 C>G variant interacts with changes in body weight over time to aggravate liver steatosis, but reduces the risk of incident type 2 diabetes.
Topics: Adipose Tissue; Aged; Anthropometry; Blood Glucose; Body Weight; China; Diabetes Mellitus, Type 2; F | 2019 |
Genetic and metabolic predictors of hepatic fat content in a cohort of Italian children with obesity.
Topics: Acyltransferases; Adaptor Proteins, Signal Transducing; Adipose Tissue; Adolescent; Alleles; Body Ma | 2019 |
Combining I148M and E167K variants to improve risk prediction for nonalcoholic fatty liver disease in Qingdao Han population, China.
Topics: Asian People; Case-Control Studies; China; Female; Gene Frequency; Genetic Association Studies; Gene | 2019 |
American Ancestry Is a Risk Factor for Suspected Nonalcoholic Fatty Liver Disease in Hispanic/Latino Adults.
Topics: Adult; Biomarkers; DNA; Female; Genetic Predisposition to Disease; Hispanic or Latino; Humans; Lipas | 2019 |
Comparative study of overweight and obese patients with nonalcoholic fatty liver disease.
Topics: Adiponectin; Adult; Analysis of Variance; Biopsy, Needle; Body Mass Index; Cross-Sectional Studies; | 2019 |
Pnpla3 silencing with antisense oligonucleotides ameliorates nonalcoholic steatohepatitis and fibrosis in Pnpla3 I148M knock-in mice.
Topics: Animals; Female; Gene Silencing; Humans; Lipase; Liver Cirrhosis; Membrane Proteins; Mice; Mice, Inb | 2019 |
Relationship Between PNPLA3 rs738409 Polymorphism and Decreased Kidney Function in Children With NAFLD.
Topics: Adolescent; Child; Child, Preschool; Cross-Sectional Studies; Female; Glomerular Filtration Rate; Hu | 2019 |
PNPLA2 influences secretion of triglyceride-rich lipoproteins by human hepatoma cells.
Topics: Blotting, Western; Cell Line, Tumor; Diglycerides; Endoplasmic Reticulum; Fatty Acids; Hep G2 Cells; | 2019 |
Effects of daphnetin on lipid metabolism, insulin resistance and oxidative stress in OA‑treated HepG2 cells.
Topics: AMP-Activated Protein Kinases; Cell Survival; Cytochrome P-450 CYP2E1; Cytochrome P-450 CYP4A; Dose- | 2019 |
The Role of Genetic Predisposition, Programing During Fetal Life, Family Conditions, and Post-natal Diet in the Development of Pediatric Fatty Liver Disease.
Topics: Birth Weight; Breast Feeding; Child; Child Nutritional Physiological Phenomena; Child, Preschool; Fa | 2019 |
Nonalcoholic fatty liver disease and eGFR levels could be linked by the PNPLA3 I148M polymorphism in children with obesity.
Topics: Adolescent; Child; Female; Genotype; Glomerular Filtration Rate; Humans; Lipase; Male; Membrane Prot | 2019 |
Genetic polymorphisms associated with obesity and non-alcoholic fatty liver disease in Asian Indian adolescents.
Topics: Adiponectin; Adolescent; Adult; Apolipoprotein C-III; Biomarkers; Case-Control Studies; Child; Femal | 2019 |
The PNPLA3 rs738409 C>G variant influences the association between low skeletal muscle mass and NAFLD: the Shanghai Changfeng Study.
Topics: Adult; Aged; Asian People; China; Female; Humans; Lipase; Male; Membrane Proteins; Middle Aged; Non- | 2019 |
Contribution of a genetic risk score to clinical prediction of hepatic steatosis in obese children and adolescents.
Topics: Adaptor Proteins, Signal Transducing; Adolescent; Child; Female; Genetic Loci; Genetic Predispositio | 2019 |
Association of Genetic Non-alcoholic Fatty Liver Disease with Insulin Resistance-Are we Different?
Topics: Diabetes Mellitus, Type 2; Humans; Insulin Resistance; Lipase; Membrane Proteins; Non-alcoholic Fatt | 2019 |
GWAS and enrichment analyses of non-alcoholic fatty liver disease identify new trait-associated genes and pathways across eMERGE Network.
Topics: Adult; Aged; Body Mass Index; Case-Control Studies; Community Networks; Disease Progression; Electro | 2019 |
Apolipoprotein B and PNPLA3 Double Heterozygosity in a Father-Son Pair With Advanced Nonalcoholic Fatty Liver Disease.
Topics: 17-Hydroxysteroid Dehydrogenases; Adaptor Proteins, Signal Transducing; Aged; Apolipoproteins B; Cho | 2020 |
Donor PNPLA3 and TM6SF2 Variant Alleles Confer Additive Risks for Graft Steatosis After Liver Transplantation.
Topics: Adult; Alleles; Allografts; Biopsy; Female; Follow-Up Studies; Genotyping Techniques; Humans; Lipase | 2020 |
PNPLA3 gene polymorphism in Brazilian patients with type 2 diabetes: A prognostic marker beyond liver disease?
Topics: Aged; Aged, 80 and over; Blood Glucose; Brazil; Cross-Sectional Studies; Diabetes Mellitus, Type 2; | 2019 |
Interactions of allelic variance of PNPLA3 with nongenetic factors in predicting nonalcoholic steatohepatitis and nonhepatic complications of severe obesity.
Topics: Adult; Alleles; Blood Glucose; C-Reactive Protein; Diabetes Mellitus, Type 1; Fatty Liver; Female; F | 2013 |
Susceptibility and gene interaction study of the angiotensin II type 1 receptor (AGTR1) gene polymorphisms with non-alcoholic fatty liver disease in a multi-ethnic population.
Topics: Asian People; Epistasis, Genetic; Fatty Liver; Genetic Predisposition to Disease; Genotype; Haplotyp | 2013 |
A gene variant of PNPLA3, but not of APOC3, is associated with histological parameters of NAFLD in an obese population.
Topics: Adult; Alanine Transaminase; Apolipoprotein C-III; Aspartate Aminotransferases; Body Mass Index; Cro | 2013 |
Genetic variation in the patatin-like phospholipase domain-containing protein-3 (PNPLA-3) gene in Asian Indians with nonalcoholic fatty liver disease.
Topics: Adult; Anthropometry; Asian People; Blood Glucose; Blood Pressure; Case-Control Studies; Cholesterol | 2013 |
Association of glucokinase regulatory gene polymorphisms with risk and severity of non-alcoholic fatty liver disease: an interaction study with adiponutrin gene.
Topics: Adult; Alleles; Case-Control Studies; Female; Gene Frequency; Genetic Predisposition to Disease; Gen | 2014 |
Genetic and clinical markers of elevated liver fat content in overweight and obese Hispanic children.
Topics: Adolescent; Alanine Transaminase; Alleles; Anthropometry; Apolipoprotein C-III; Aspartate Aminotrans | 2013 |
Oxidized fatty acids: A potential pathogenic link between fatty liver and type 2 diabetes in obese adolescents?
Topics: Adolescent; Biomarkers; Child; Diabetes Mellitus, Type 2; Fatty Acids; Fatty Liver; Female; Glucose; | 2014 |
Adipocyte size is associated with NAFLD independent of obesity, fat distribution, and PNPLA3 genotype.
Topics: Adipocytes; Adult; Body Composition; Body Fat Distribution; Cross-Sectional Studies; Fatty Liver; Fe | 2013 |
Role of adipose triglyceride lipase (PNPLA2) in protection from hepatic inflammation in mouse models of steatohepatitis and endotoxemia.
Topics: Animals; Choline Deficiency; Disease Models, Animal; Endotoxemia; Fatty Liver; Female; Lipase; Lipop | 2014 |
PNPLA3 GG genotype and carotid atherosclerosis in patients with non-alcoholic fatty liver disease.
Topics: Adult; Aged; Alleles; Carotid Arteries; Carotid Artery Diseases; Fatty Liver; Female; Genetic Associ | 2013 |
[Polymorphism rs738409 in PNPLA3 is associated with inherited susceptibility to non-alcoholic fatty liver disease].
Topics: Adolescent; Adult; Aged; Alleles; Case-Control Studies; Fatty Liver; Female; Gene Frequency; Genetic | 2013 |
PNPLA3 I148M polymorphism, clinical presentation, and survival in patients with hepatocellular carcinoma.
Topics: Aged; Carcinoma, Hepatocellular; Case-Control Studies; Demography; Fatty Liver; Female; Follow-Up St | 2013 |
A population-based study on the prevalence of NASH using scores validated against liver histology.
Topics: Adolescent; Adult; Aged; Biopsy; Cohort Studies; Diabetes Mellitus, Type 2; Female; Finland; Humans; | 2014 |
A 4-polymorphism risk score predicts steatohepatitis in children with nonalcoholic fatty liver disease.
Topics: Adolescent; Biopsy; Child; Female; Genetic Predisposition to Disease; Humans; Kruppel-Like Factor 6; | 2014 |
No correlation between PNPLA3 rs738409 genotype and fatty liver and hepatic cirrhosis in Japanese patients with HCV.
Topics: Adult; Aged; Asian People; Fatty Liver; Female; Genetic Predisposition to Disease; Genotype; Hepaciv | 2013 |
PNPLA3 gene polymorphism accounts for fatty liver in community subjects without metabolic syndrome.
Topics: Adult; Diet; Fatty Liver; Female; Humans; Lipase; Male; Membrane Proteins; Metabolic Syndrome; Middl | 2014 |
Therapeutic role of ursolic acid on ameliorating hepatic steatosis and improving metabolic disorders in high-fat diet-induced non-alcoholic fatty liver disease rats.
Topics: Animals; CD36 Antigens; Diacylglycerol O-Acyltransferase; Diet, High-Fat; Dietary Fats; Fatty Liver; | 2014 |
Glucokinase regulatory protein gene polymorphism affects liver fibrosis in non-alcoholic fatty liver disease.
Topics: Adaptor Proteins, Signal Transducing; Adult; Female; Gene Frequency; Genetic Predisposition to Disea | 2014 |
Role of adipose tissue in methionine-choline-deficient model of non-alcoholic steatohepatitis (NASH).
Topics: Adipogenesis; Adipose Tissue; Animals; Choline; Disease Models, Animal; Fatty Acids; Fatty Acids, No | 2014 |
Carriage of the PNPLA3 rs738409 C >G polymorphism confers an increased risk of non-alcoholic fatty liver disease associated hepatocellular carcinoma.
Topics: Adult; Aged; Carcinoma, Hepatocellular; Case-Control Studies; Cohort Studies; Disease Progression; F | 2014 |
Targeted next-generation sequencing and fine linkage disequilibrium mapping reveals association of PNPLA3 and PARVB with the severity of nonalcoholic fatty liver disease.
Topics: Actinin; Adult; Aged; Biopsy; Case-Control Studies; Chromosome Mapping; Disease Progression; Female; | 2014 |
Commentary: dissecting the PNPLA3 association with liver fat and stiffness, and interaction with diet.
Topics: Fatty Liver; Female; Humans; Lipase; Male; Membrane Proteins; Non-alcoholic Fatty Liver Disease | 2014 |
Commentary: dissecting the PNPLA3 association with liver fat and stiffness, and interaction with diet - authors' reply.
Topics: Fatty Liver; Female; Humans; Lipase; Male; Membrane Proteins; Non-alcoholic Fatty Liver Disease | 2014 |
Risk factors for fatty liver in the Multicenter AIDS Cohort Study.
Topics: Anti-HIV Agents; Case-Control Studies; Cohort Studies; Cross-Sectional Studies; Fatty Liver; Genetic | 2014 |
PNPLA3 has retinyl-palmitate lipase activity in human hepatic stellate cells.
Topics: Adult; Diterpenes; Female; Gene Expression Regulation; Hep G2 Cells; Hepatic Stellate Cells; Humans; | 2014 |
Lack of association between apolipoprotein C3 gene polymorphisms and risk of nonalcoholic fatty liver disease in a Chinese Han population.
Topics: Adult; Aged; Alleles; Antioxidants; Apolipoprotein C-III; Case-Control Studies; China; Female; Gene | 2014 |
Association of polymorphisms in GCKR and TRIB1 with nonalcoholic fatty liver disease and metabolic syndrome traits.
Topics: Adaptor Proteins, Signal Transducing; Adult; Alleles; Case-Control Studies; Female; Gene Frequency; | 2014 |
Oxidative stress and altered lipid homeostasis in the programming of offspring fatty liver by maternal obesity.
Topics: Adiposity; Age Factors; Animal Nutritional Physiological Phenomena; Animals; Body Weight; Cytochrome | 2014 |
Genetic variants in the PNPLA3 gene are associated with nonalcoholic steatohepatitis.
Topics: Case-Control Studies; Gene Frequency; Genetic Markers; Genetic Predisposition to Disease; Genotype; | 2014 |
Non-alcoholic fatty liver disease, metabolic syndrome and patatin-like phospholipase domain-containing protein3 gene variants.
Topics: Adult; Aged; Cardiovascular Diseases; Cohort Studies; Female; Genetic Predisposition to Disease; Hum | 2014 |
NAFLD. PNPLA3 variant and hepatic steatosis.
Topics: Fatty Liver; Genetic Variation; Humans; Lipase; Membrane Proteins; Non-alcoholic Fatty Liver Disease | 2014 |
Role of the PNPLA3 I148M polymorphism in nonalcoholic fatty liver disease and fibrosis in Korea.
Topics: Adult; Case-Control Studies; Female; Genetic Predisposition to Disease; Genotype; Humans; Lipase; Li | 2014 |
Association between genetic variants in PNPLA3 and serum adiponectin.
Topics: Adiponectin; Blood Chemical Analysis; Cohort Studies; Female; Genetic Predisposition to Disease; Ger | 2015 |
Association between the PNPLA3 I148M polymorphism and non-alcoholic fatty liver disease in the Uygur and Han ethnic groups of northwestern China.
Topics: Adult; Alleles; Case-Control Studies; China; Female; Gene-Environment Interaction; Genetic Associati | 2014 |
Noninvasive characterization of graft steatosis after liver transplantation.
Topics: Adult; Aged; Alleles; Body Mass Index; Cohort Studies; Diabetes Mellitus; Elasticity Imaging Techniq | 2015 |
Circulating triacylglycerol signatures and insulin sensitivity in NAFLD associated with the E167K variant in TM6SF2.
Topics: Adipose Tissue; Adult; Amino Acid Substitution; Female; Finland; Gene Frequency; Genetic Association | 2015 |
GWAS-Identified Common Variants With Nonalcoholic Fatty Liver Disease in Chinese Children.
Topics: Adaptor Proteins, Signal Transducing; Adolescent; Alanine Transaminase; Asian People; Case-Control S | 2015 |
HCC and liver disease risks in homozygous PNPLA3 p.I148M carriers approach monogenic inheritance.
Topics: Carcinoma, Hepatocellular; Female; Humans; Lipase; Liver Neoplasms; Male; Membrane Proteins; Non-alc | 2015 |
Reply to: HCC and liver disease risk in homozygous PNPLA3 p.I148M carriers approach monogenic inheritance.
Topics: Carcinoma, Hepatocellular; Female; Humans; Lipase; Liver Neoplasms; Male; Membrane Proteins; Non-alc | 2015 |
TM6SF2 E167K variant is associated with severe steatosis in chronic hepatitis C, regardless of PNPLA3 polymorphism.
Topics: Adult; Analysis of Variance; Antiviral Agents; Cohort Studies; Female; Genetic Predisposition to Dis | 2015 |
A genetic risk score is associated with hepatic triglyceride content and non-alcoholic steatohepatitis in Mexicans with morbid obesity.
Topics: Adaptor Proteins, Signal Transducing; Adult; Cholesterol; Chondroitin Sulfate Proteoglycans; Female; | 2015 |
The SRE Motif in the Human PNPLA3 Promoter (-97 to -88 bp) Mediates Transactivational Effects of SREBP-1c.
Topics: CCAAT-Binding Factor; Gene Expression Regulation; Hep G2 Cells; Humans; Insulin; Lipase; Liver; Memb | 2015 |
Role of fibroblast growth factor 21 in the early stage of NASH induced by methionine- and choline-deficient diet.
Topics: Adipocytes, White; Animals; CD36 Antigens; Cells, Cultured; Choline Deficiency; Diet; Endoplasmic Re | 2015 |
Targeted-bisulfite sequence analysis of the methylation of CpG islands in genes encoding PNPLA3, SAMM50, and PARVB of patients with non-alcoholic fatty liver disease.
Topics: Actinin; CpG Islands; DNA; DNA Methylation; Female; Genetic Predisposition to Disease; Genotype; Hum | 2015 |
PNPLA3 rs738409 I748M is associated with steatohepatitis in 434 non-obese subjects with hepatitis C.
Topics: Adult; Cohort Studies; Fatty Liver; Female; Genotype; Hepacivirus; Hepatitis C, Chronic; Humans; Lip | 2015 |
[Association between patatin-like phospholipase domain-containing protein 3 gene rs738409 polymorphism and non-alcoholic fatty liver disease susceptibility: a meta-analysis].
Topics: Asian People; Case-Control Studies; Disease Susceptibility; Fatty Liver; Genetic Predisposition to D | 2015 |
TM6SF2 Glu167Lys polymorphism is associated with low levels of LDL-cholesterol and increased liver injury in obese children.
Topics: Adolescent; Alanine Transaminase; Alleles; Child; Cholesterol, HDL; Cholesterol, LDL; Female; Geneti | 2016 |
Patatin-like phospholipase 3 (rs738409) gene polymorphism is associated with increased liver enzymes in obese adolescents and metabolic syndrome in all ages.
Topics: Adolescent; Adult; Aged; Alleles; Case-Control Studies; Child; Female; Genotype; Heterozygote; Human | 2015 |
Salicylic acid elicitation during cultivation of the peppermint plant improves anti-diabetic effects of its infusions.
Topics: Animals; Diabetes Mellitus, Experimental; Dietary Supplements; Enzyme Inhibitors; Fertilizers; Gastr | 2015 |
Statin use and non-alcoholic steatohepatitis in at risk individuals.
Topics: Adult; Aged; Biopsy; Female; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Lipase; Liver; | 2015 |
Characterization of lipid metabolism in a novel immortalized human hepatocyte cell line.
Topics: Cell Line; Endoplasmic Reticulum Stress; Fatty Acids; Glucose; Hep G2 Cells; Hepatocytes; Humans; In | 2015 |
PNPLA3 I148M Variant Influences Circulating Retinol in Adults with Nonalcoholic Fatty Liver Disease or Obesity.
Topics: Aged; Female; Genetic Variation; Humans; Lipase; Male; Membrane Proteins; Middle Aged; Non-alcoholic | 2015 |
I148M variant in PNPLA3 reduces central adiposity and metabolic disease risks while increasing nonalcoholic fatty liver disease.
Topics: Adult; Body Mass Index; Genetic Predisposition to Disease; Humans; Insulin Resistance; Lipase; Liver | 2015 |
Influence of the PNPLA3 rs738409 Polymorphism on Non-Alcoholic Fatty Liver Disease and Renal Function among Normal Weight Subjects.
Topics: Aged; Asian People; Cross-Sectional Studies; Female; Genetic Predisposition to Disease; Glomerular F | 2015 |
The fat droplet in hepatocellular ballooning and implications for scoring nonalcoholic steatohepatitis therapeutic response.
Topics: Animals; Carotid Artery Diseases; Fatty Liver; Female; Hedgehog Proteins; Humans; Lipase; Lipoprotei | 2016 |
Linked PNPLA3 polymorphisms confer susceptibility to nonalcoholic steatohepatitis and decreased viral load in chronic hepatitis B.
Topics: Adult; Asian People; Biomarkers; Biopsy; Case-Control Studies; China; DNA, Viral; Female; Gene Frequ | 2015 |
Letter: PNPLA3, metabolic syndrome and NAFLD status in obese subjects--authors' reply.
Topics: Female; Humans; Lipase; Male; Membrane Proteins; Metabolic Syndrome; Non-alcoholic Fatty Liver Disea | 2015 |
Letter: PNPLA3, metabolic syndrome and NAFLD status in obese subjects.
Topics: Female; Humans; Lipase; Male; Membrane Proteins; Metabolic Syndrome; Non-alcoholic Fatty Liver Disea | 2015 |
TM6SF2 rs58542926 is not associated with steatosis and fibrosis in large cohort of patients with genotype 1 chronic hepatitis C.
Topics: Adult; Cohort Studies; Fatty Liver; Female; Hepatitis C, Chronic; Humans; Interferons; Interleukins; | 2016 |
The common PNPLA3 variant p.I148M is associated with liver fat contents as quantified by controlled attenuation parameter (CAP).
Topics: Adiposity; Adolescent; Adult; Aged; Body Mass Index; Case-Control Studies; Elasticity Imaging Techni | 2016 |
PNPLA3 148M Carriers with Inflammatory Bowel Diseases Have Higher Susceptibility to Hepatic Steatosis and Higher Liver Enzymes.
Topics: Alanine Transaminase; Alleles; Aspartate Aminotransferases; Biomarkers; Cohort Studies; Disease Prog | 2016 |
PNPLA3 I148M variant affects non-alcoholic fatty liver disease in liver transplant recipients.
Topics: Adult; Asian People; China; Cross-Sectional Studies; Female; Gene Frequency; Genetic Association Stu | 2015 |
Diet-Quality Scores and Prevalence of Nonalcoholic Fatty Liver Disease: A Population Study Using Proton-Magnetic Resonance Spectroscopy.
Topics: Adult; Aged; Asian People; Cross-Sectional Studies; Diet Records; Diet Surveys; Diet, Mediterranean; | 2015 |
Hepatic lipase deficiency produces glucose intolerance, inflammation and hepatic steatosis.
Topics: Animals; Blood Glucose; Chemokine CCL2; Diet, High-Fat; Dyslipidemias; Glucose Intolerance; Inflamma | 2015 |
The Impact of PNPLA3 rs738409 Genetic Polymorphism and Weight Gain ≥10 kg after Age 20 on Non-Alcoholic Fatty Liver Disease in Non-Obese Japanese Individuals.
Topics: Adult; Aged; Alanine Transaminase; Alleles; Asian People; Aspartate Aminotransferases; Body Mass Ind | 2015 |
Association study of PNPLA2 gene with histological parameters of NAFLD in an obese population.
Topics: Adult; Belgium; Female; Humans; Linear Models; Lipase; Male; Non-alcoholic Fatty Liver Disease; Obes | 2016 |
The rs2294918 E434K variant modulates patatin-like phospholipase domain-containing 3 expression and liver damage.
Topics: Adolescent; Adult; Alanine Transaminase; Case-Control Studies; Child; Female; Genetic Predisposition | 2016 |
Relationships between Genetic Variations of PNPLA3, TM6SF2 and Histological Features of Nonalcoholic Fatty Liver Disease in Japan.
Topics: Adult; Aged; Aged, 80 and over; Female; Genotype; Humans; Lipase; Liver Cirrhosis; Male; Membrane Pr | 2016 |
Multi-omic profiles of human non-alcoholic fatty liver disease tissue highlight heterogenic phenotypes.
Topics: Apolipoprotein C-III; Biopsy; Chondroitin Sulfate Proteoglycans; Genetic Association Studies; Geneti | 2015 |
Association of PNPLA3 Polymorphism with Hepatocellular Carcinoma Development and Prognosis in Viral and Non-Viral Chronic Liver Diseases.
Topics: Aged; Carcinoma, Hepatocellular; Case-Control Studies; Disease Progression; Fatty Liver, Alcoholic; | 2015 |
Reduction of Caloric Intake Might Override the Prosteatotic Effects of the PNPLA3 p.I148M and TM6SF2 p.E167K Variants in Patients with Fatty Liver: Ultrasound-Based Prospective Study.
Topics: Adolescent; Adult; Aged; Alleles; Case-Control Studies; Diet, Reducing; Female; Genetic Predispositi | 2016 |
I148M variant of PNPLA3 increases the susceptibility to non-alcoholic fatty liver disease caused by obesity and metabolic disorders.
Topics: Aged; Alleles; Blood Glucose; Body Mass Index; Body Weights and Measures; Carotid Intima-Media Thick | 2016 |
Association of PNPLA3 rs738409 and TM6SF2 rs58542926 with health services utilization in a population-based study.
Topics: Adult; Aged; Disease Progression; Female; Genotype; Germany; Health Services; Humans; Lipase; Male; | 2016 |
Depletion of Rab32 decreases intracellular lipid accumulation and induces lipolysis through enhancing ATGL expression in hepatocytes.
Topics: Gene Knockdown Techniques; Hep G2 Cells; Hepatocytes; Humans; Lipase; Lipid Metabolism; Lipolysis; N | 2016 |
Interactions of a PPARGC1A Variant and a PNPLA3 Variant Affect Nonalcoholic Steatohepatitis in Severely Obese Taiwanese Patients.
Topics: Adaptor Proteins, Signal Transducing; Adult; Alleles; Bariatric Surgery; Biopsy; Female; Genetic Pre | 2016 |
APOC3 rs2070666 Is Associated with the Hepatic Steatosis Independently of PNPLA3 rs738409 in Chinese Han Patients with Nonalcoholic Fatty Liver Diseases.
Topics: Adult; Alanine Transaminase; Apolipoprotein C-III; Asian People; Body Mass Index; Case-Control Studi | 2016 |
PNPLA3 Expression Is Related to Liver Steatosis in Morbidly Obese Women with Non-Alcoholic Fatty Liver Disease.
Topics: Alleles; Cohort Studies; Female; Genotype; Humans; Lipase; Lipid Metabolism; Liver; Liver X Receptor | 2016 |
The PNPLA3 rs738409 C > G polymorphism is associated with the risk of progression to cirrhosis in NAFLD patients.
Topics: Adult; Female; Gene Frequency; Humans; Lipase; Liver; Liver Cirrhosis; Male; Membrane Proteins; Midd | 2016 |
Screening for rare variants in the PNPLA3 gene in obese liver biopsy patients.
Topics: Adult; Biopsy; DNA Mutational Analysis; Female; Humans; Lipase; Liver; Male; Membrane Proteins; Non- | 2016 |
Effects of the new thiazolidine derivative LPSF/GQ-02 on hepatic lipid metabolism pathways in non-alcoholic fatty liver disease (NAFLD).
Topics: Acetyl-CoA Carboxylase; AMP-Activated Protein Kinases; Animals; Fatty Acid Synthases; Forkhead Box P | 2016 |
Association of MBOAT7 gene variant with plasma ALT levels in children: the PANIC study.
Topics: Acyltransferases; Alanine Transaminase; Alleles; Child; Female; Follow-Up Studies; Genetic Associati | 2016 |
[Influence of leptin receptor gene K109R polymorphism on the risk of nonalcoholic fatty liver disease and its interaction with PNPLA3 I148M polymorphism].
Topics: Alleles; Asian People; Case-Control Studies; China; Genetic Predisposition to Disease; Genotype; Hum | 2016 |
Weight loss induced by bariatric surgery restores adipose tissue PNPLA3 expression.
Topics: Adipose Tissue; Adult; Aged; Austria; Bariatric Surgery; Female; Hepatocytes; Humans; Laparoscopy; L | 2017 |
Association of patatin-like phospholipase domain-containing protein 3 gene polymorphisms with susceptibility of nonalcoholic fatty liver disease in a Han Chinese population.
Topics: Asian People; Case-Control Studies; China; Female; Genetic Predisposition to Disease; Humans; Lipase | 2016 |
PNPLA3 p.I148M variant is associated with greater reduction of liver fat content after bariatric surgery.
Topics: Adipose Tissue; Adult; Analysis of Variance; Bariatric Surgery; Female; Humans; Lipase; Lipid Metabo | 2016 |
The role of mitochondrial genomics in patients with non-alcoholic steatohepatitis (NASH).
Topics: Adult; Biopsy; Female; Genetic Predisposition to Disease; Genome, Mitochondrial; Genomics; Haplotype | 2016 |
Transcriptional regulation of PNPLA3 and its impact on susceptibility to nonalcoholic fatty liver Disease (NAFLD) in humans.
Topics: Adult; Alleles; Case-Control Studies; Female; Gene Expression Regulation; Genetic Predisposition to | 2016 |
LncRNA SRA promotes hepatic steatosis through repressing the expression of adipose triglyceride lipase (ATGL).
Topics: Animals; Carrier Proteins; Diet, High-Fat; Fasting; Fatty Liver; Forkhead Box Protein O1; Gene Expre | 2016 |
Combined effects of the PNPLA3 rs738409, TM6SF2 rs58542926, and MBOAT7 rs641738 variants on NAFLD severity: a multicenter biopsy-based study.
Topics: Acyltransferases; Adolescent; Adult; Aged; Aged, 80 and over; Alleles; Biopsy; Fatty Liver; Female; | 2017 |
Patatin-like phospholipase domain-containing protein 3 (PNPLA3): A potential role in the association between liver disease and bipolar disorder.
Topics: Adolescent; Adult; Bipolar Disorder; Female; Genetic Predisposition to Disease; Genotype; Humans; Li | 2017 |
Physical activity and sedentary behavior can modulate the effect of the PNPLA3 variant on childhood NAFLD: a case-control study in a Chinese population.
Topics: Adolescent; Asian People; Case-Control Studies; Child; Exercise; Female; Genetic Predisposition to D | 2016 |
Low hepatic copper content and PNPLA3 polymorphism in non-alcoholic fatty liver disease in patients without metabolic syndrome.
Topics: Adult; Copper; Female; Humans; Lipase; Liver; Male; Membrane Proteins; Metabolic Syndrome; Middle Ag | 2017 |
Obesity/insulin resistance rather than liver fat increases coagulation factor activities and expression in humans.
Topics: Adipose Tissue; Adiposity; Adult; Biomarkers; Biopsy; Blood Coagulation; Blood Coagulation Factors; | 2017 |
Non-alcoholic fatty liver disease and subclinical atherosclerosis: A comparison of metabolically- versus genetically-driven excess fat hepatic storage.
Topics: Adult; Asymptomatic Diseases; Carotid Artery Diseases; Carotid Artery, Common; Carotid Intima-Media | 2017 |
PNPLA3, TM6SF2, and MBOAT7 Genotypes and Coronary Artery Disease.
Topics: Acyltransferases; Case-Control Studies; Coronary Artery Disease; Databases, Genetic; Gene Frequency; | 2017 |
The association of nonalcoholic fatty liver disease with genetic polymorphisms: a multicenter study.
Topics: Adolescent; Adult; Aged; Case-Control Studies; Genetic Predisposition to Disease; Humans; Image-Guid | 2017 |
Distinct regulation of adiponutrin/PNPLA3 gene expression by the transcription factors ChREBP and SREBP1c in mouse and human hepatocytes.
Topics: Animals; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; Binding Sites; Fatty Liver; Ge | 2011 |
A common variant in the PNPLA3 gene is a risk factor for non-alcoholic fatty liver disease in obese Taiwanese children.
Topics: Adolescent; Alleles; Child; DNA; Fatty Liver; Female; Genetic Predisposition to Disease; Genotype; H | 2011 |
Association of the rs738409 polymorphism in PNPLA3 with liver damage and the development of nonalcoholic fatty liver disease.
Topics: Adult; Age Factors; Aged; Alanine Transaminase; Alleles; Aspartate Aminotransferases; Body Mass Inde | 2010 |
Association of PNPLA3 with non-alcoholic fatty liver disease in a minority cohort: the Insulin Resistance Atherosclerosis Family Study.
Topics: Adolescent; Adult; Aged; Aged, 80 and over; Atherosclerosis; Black or African American; Cohort Studi | 2011 |
Methodological concerns about a recent meta-analysis of the influence of the I148M variant of patatin-like phospholipase domain containing 3 on the susceptibility and histological severity of nonalcoholic fatty liver disease.
Topics: Fatty Liver; Genetic Predisposition to Disease; Genetic Variation; Humans; Lipase; Membrane Proteins | 2011 |
Association of PNPLA3 SNP rs738409 with liver density in African Americans with type 2 diabetes mellitus.
Topics: Aged; Black or African American; Diabetes Mellitus, Type 2; Fatty Liver; Female; Humans; Lipase; Liv | 2011 |
APOC3 polymorphisms and non-alcoholic fatty liver disease: resolving some doubts and raising others.
Topics: Apolipoprotein C-III; Fatty Liver; Female; Humans; Lipase; Male; Membrane Proteins; Non-alcoholic Fa | 2011 |
First European Young Hepatologist Workshop: topics and advances.
Topics: Carcinoma, Hepatocellular; End Stage Liver Disease; European Union; Fatty Liver; Genetic Markers; Hu | 2011 |
The PNPLA3 I148M polymorphism is associated with insulin resistance and nonalcoholic fatty liver disease in a normoglycaemic population.
Topics: Adult; Analysis of Variance; Biomarkers; Blood Glucose; Case-Control Studies; Chi-Square Distributio | 2011 |
PNPLA3 rs738409C/G polymorphism in cirrhosis: relationship with the aetiology of liver disease and hepatocellular carcinoma occurrence.
Topics: Adult; Aged; Aged, 80 and over; Carcinoma, Hepatocellular; Case-Control Studies; Chi-Square Distribu | 2011 |
PNPLA3 polymorphism influences liver fibrosis in unselected patients with type 2 diabetes.
Topics: Aged; Biomarkers; Body Mass Index; Chi-Square Distribution; Cross-Sectional Studies; Diabetes Mellit | 2011 |
The SOD2 C47T polymorphism influences NAFLD fibrosis severity: evidence from case-control and intra-familial allele association studies.
Topics: Adult; Base Sequence; Case-Control Studies; Cohort Studies; DNA Primers; Family; Fatty Liver; Female | 2012 |
The APOC3 T-455C and C-482T promoter region polymorphisms are not associated with the severity of liver damage independently of PNPLA3 I148M genotype in patients with nonalcoholic fatty liver.
Topics: Adolescent; Adult; Apolipoprotein C-III; Base Sequence; Case-Control Studies; Child; DNA Primers; Fa | 2011 |
The metabolically benign and malignant fatty liver.
Topics: Animals; Cardiovascular Diseases; Child; Diabetes Mellitus, Type 1; Fatty Liver; Hepatitis; Humans; | 2011 |
Expression and characterization of a PNPLA3 protein isoform (I148M) associated with nonalcoholic fatty liver disease.
Topics: Acyl Coenzyme A; Amino Acid Substitution; Cell Line; Fatty Liver; Humans; Hydrolysis; Isoenzymes; Li | 2011 |
Genetic variant in PNPLA3 is associated with nonalcoholic fatty liver disease in China.
Topics: Adult; China; Fatty Liver; Female; Genetic Predisposition to Disease; Genetic Variation; Humans; Lip | 2012 |
Serum interleukin 1 receptor antagonist as an independent marker of non-alcoholic steatohepatitis in humans.
Topics: Adult; Aged; Alanine Transaminase; Biomarkers; Biopsy; Fatty Liver; Female; Genotype; Humans; Insuli | 2012 |
Understanding the relationship between PNPLA3, NAFLD and insulin resistance: do ethnic differences bring more questions or more answers?
Topics: Blood Glucose; Diabetes Mellitus, Type 2; Fatty Liver; Female; Humans; Insulin Resistance; Lipase; L | 2011 |
Genetic variation in PNPLA3 but not APOC3 influences liver fat in non-alcoholic fatty liver disease.
Topics: Adult; Age Factors; Alanine Transaminase; Alleles; Analysis of Variance; Apolipoprotein C-III; Aspar | 2012 |
A multi-ethnic study of a PNPLA3 gene variant and its association with disease severity in non-alcoholic fatty liver disease.
Topics: Alleles; Body Mass Index; Case-Control Studies; Fatty Liver; Female; Gene Frequency; Genetic Predisp | 2012 |
Absence of adipose triglyceride lipase protects from hepatic endoplasmic reticulum stress in mice.
Topics: Animals; Blotting, Western; Cells, Cultured; Cholesterol; Disease Models, Animal; Endoplasmic Reticu | 2012 |
IL28B and PNPLA3 polymorphisms affect histological liver damage in patients with non-alcoholic fatty liver disease.
Topics: Adult; Cross-Sectional Studies; Fatty Liver; Female; Humans; Interferons; Interleukins; Lipase; Live | 2012 |
APOC3 and PNPLA3 in non-alcoholic fatty liver disease: need to clear the air.
Topics: Apolipoprotein C-III; Fatty Liver; Female; Humans; Lipase; Male; Membrane Proteins; Non-alcoholic Fa | 2012 |
Hepatic lipase activity is increased in non-alcoholic fatty liver disease beyond insulin resistance.
Topics: Atherosclerosis; Cardiovascular Diseases; Fatty Liver; Humans; Insulin Resistance; Lipase; Liver; No | 2012 |
Alpha-lipoic acid induces adipose triglyceride lipase expression and decreases intracellular lipid accumulation in HepG2 cells.
Topics: Active Transport, Cell Nucleus; AMP-Activated Protein Kinases; Cell Nucleus; Enzyme Activation; Fatt | 2012 |
PNPLA3, a genetic marker of progressive liver disease, still hiding its metabolic function?
Topics: Disease Progression; Fatty Liver; Genetic Markers; Humans; Lipase; Membrane Proteins; Non-alcoholic | 2013 |
The interaction of rs738409, obesity, and alcohol: a population-based autopsy study.
Topics: Accidents, Traffic; Adult; Autopsy; Fatty Liver; Fatty Liver, Alcoholic; Female; Genotype; Humans; K | 2012 |
PNPLA3, the triacylglycerol synthesis/hydrolysis/storage dilemma, and nonalcoholic fatty liver disease.
Topics: Animals; Fatty Liver; Genetic Predisposition to Disease; Humans; Lipase; Lipogenesis; Lipolysis; Liv | 2012 |
Genetic variant I148M in PNPLA3 is associated with the ultrasonography-determined steatosis degree in a Chinese population.
Topics: Adult; Asian People; Fatty Liver; Female; Gene Frequency; Genetic Predisposition to Disease; Humans; | 2012 |
Genetic variants in PNPLA3 and risk of non-alcoholic fatty liver disease in a Han Chinese population.
Topics: Adult; Alleles; Asian People; Case-Control Studies; Fatty Liver; Female; Genetic Predisposition to D | 2012 |
Adipose tissue is inflamed in NAFLD due to obesity but not in NAFLD due to genetic variation in PNPLA3.
Topics: Adiponectin; Adipose Tissue; Adult; Body Composition; Fatty Liver; Female; Gene Expression Regulatio | 2013 |