epiglucan has been researched along with Non-alcoholic-Fatty-Liver-Disease* in 7 studies
1 trial(s) available for epiglucan and Non-alcoholic-Fatty-Liver-Disease
Article | Year |
---|---|
Novel nutraceutical supplements with yeast β-glucan, prebiotics, minerals, and
It is known that obesity has a multifactorial etiology that involves genetic and environmental factors. The WHO estimates the worldwide prevalence of 1.9 billion overweight adults and more than 650 million people with obesity. These alarming data highlight the high and growing prevalence of obesity and represent a risk factor for the development and aggravation of other chronic diseases, such as nonalcoholic fatty liver disease (NAFLD) that is frequently considered the hepatic outcome of type 2 diabetes. The use of non-pharmacological therapies such as food supplements, nutraceuticals, and natural integrative therapies has grown as an alternative tool for obesity-related diseases compared to conventional medications. However, it is a still little explored research field and lacks scientific evidence of therapeutic effectiveness. Considering this, the aim is to evaluate whether a new nutraceutical supplement composition can improve and supply essential mineral nutrients, providing an improvement of obesity-related metabolic and endocrine parameters.. Sedentary volunteers (women and men) with body mass index (BMI) ≤34.9 kg/m. In the anthropometric analysis, the waist circumference in middle abdomen (WC-mid) and waist circumference in iliac crest (WC-IC) were reduced. Also, the waist-to-height ratio (WHt R) and waist-to-hip ratio (WHR) seem to slightly decrease alongside the supplementation period with both nutraceutical supplements tested as well as transaminase enzyme ratio [aspartate aminotransferase (AST)/alanine aminotransferase (ALT) ratio (AAR)], a known as a biomarker of NAFLD, and endocrine hormones cortisol and thyroid-stimulating hormone (TSH) at 90 and 180 days post-supplementation.. In a condition associated with sedentary and no nutritional intervention, the new nutraceutical supplement composition demonstrated the ability to be a strong and newfangled tool to improve important biomarkers associated with obesity and its comorbidities. Topics: Adult; beta-Glucans; Biomarkers; Diabetes Mellitus, Type 2; Dietary Supplements; Female; Humans; Male; Minerals; Non-alcoholic Fatty Liver Disease; Obesity; Prebiotics; Saccharomyces cerevisiae; Silybum marianum; Silymarin | 2022 |
6 other study(ies) available for epiglucan and Non-alcoholic-Fatty-Liver-Disease
Article | Year |
---|---|
Highland barley β-glucan alleviated western diet-induced non-alcoholic fatty liver disease
Non-alcoholic fatty liver disease (NAFLD) has become a public health burden. Controlling bile acids (BAs) metabolism and energy expenditure are potential therapies for NAFLD. Because one of the main health effects of cereal β-glucan (BG) is its ability to lower cholesterol by interacting with BAs, BG may regulate imbalances of the metabolism of BAs during NAFLD. Therefore, by using metabolic tests coupled with the profiling of hepatic BAs, we have assessed the effect of BG from highland barley on western diet (WD) induced NAFLD mice. BG treatment prevented fat accumulation and increased adipose lipolysis. These moderating effects were associated with an increased energy expenditure. Moreover, BG-treated mice enhanced the production of hepatic BAs, which may be connected with the activation of farnesoid X receptor (FXR) signaling in the liver and inhibition of FXR signaling in the ileum. Our results suggest that BG prevents fat accumulation by increasing energy expenditure, a mechanism associated with major changes in the composition of hepatic BAs. Topics: Animals; beta-Glucans; Bile Acids and Salts; Diet, Western; Energy Metabolism; Hordeum; Lipid Metabolism; Liver; Mice; Mice, Inbred C57BL; Non-alcoholic Fatty Liver Disease | 2022 |
Hepatic Lipidomics Analysis Reveals the Ameliorative Effects of Highland Barley β-Glucan on Western Diet-Induced Nonalcoholic Fatty Liver Disease Mice.
Nonalcoholic fatty liver disease (NAFLD) is characterized by marked imbalances in lipid storage and metabolism. Because the beneficial health effects of cereal β-glucan (BG) include lowering cholesterol and regulating lipid metabolism, BG may alleviate the imbalances in lipid metabolism observed during NAFLD. The aim of our study was to investigate whether BG from highland barley has an effect on western diet-induced NAFLD in mice. Using lipidomics, we investigated the underlying mechanisms of BG intervention, and identified potential lipid biomarkers. The results reveal that BG (300 mg/kg body weight) significantly alleviated liver steatosis. Lipidomics analysis demonstrated that BG also altered lipid metabolic patterns. We were able to identify 13 differentially regulated lipid species that may be useful as lipid biomarkers. Several genes in the hepatic lipid and cholesterol metabolism pathways were also modulated. These findings provide evidence that BG ameliorates NAFLD by altering liver lipid metabolites and regulating lipid metabolism-related genes. Topics: Animals; beta-Glucans; Diet, High-Fat; Diet, Western; Disease Models, Animal; Hordeum; Lipid Metabolism; Lipidomics; Liver; Mice; Mice, Inbred C57BL; Non-alcoholic Fatty Liver Disease | 2021 |
Lactobacillus rhamnosus GG and Oat Beta-Glucan Regulated Fatty Acid Profiles along the Gut-Liver-Brain Axis of Mice Fed with High Fat Diet and Demonstrated Antioxidant and Anti-Inflammatory Potentials.
This study takes a novel approach to investigate the anti-inflammatory and antioxidant effects of prebiotic oat beta-glucan (OAT) and the probiotic Lactobacillus rhamnosus GG (LGG) against high-fat diets (HFD) by examining the fatty acid profiles in the gut-liver-brain axis.. HFD-fed C57BL/6N mice are supplemented with OAT and/or LGG for 17 weeks. Thereafter, mass spectrometry-based targeted lipidomics is employed to quantify short-chain fatty acids (SCFA), polyunsaturated fatty acids (PUFA), and oxidized PUFA products in the tissues. Acetate levels are suppressed by HFD in all tissues but reversed in the brain and liver by supplementation with LGG, OAT, or LGG + OAT, and in cecum content by LGG. The n-6/n-3 polyunsaturated fatty acid (PUFA) ratio is elevated by HFD in all tissues but is lowered by LGG and OAT in the cecum and the brain, and by LGG + OAT in the brain, suggesting the anti-inflammatory property of LGG and OAT. LGG and OAT synergistically, but not individually attenuate the increase in non-enzymatic oxidized products, indicating their synbiotic antioxidant property.. The regulation of the fatty acid profiles by LGG and OAT, although incomplete, but demonstrates their anti-inflammatory and antioxidant potentials in the gut-liver-brain axis against HFD. Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Antioxidants; Avena; beta-Glucans; Brain; Caco-2 Cells; Diet, High-Fat; Dietary Supplements; Eating; Endotoxemia; Fatty Acids, Volatile; Humans; Lacticaseibacillus rhamnosus; Lipopolysaccharides; Liver; Male; Mice, Inbred C57BL; Non-alcoholic Fatty Liver Disease; Probiotics | 2020 |
Dietary salecan reverts partially the metabolic gene expressions and NMR-based metabolomic profiles from high-fat-diet-induced obese rats.
Previous studies suggest that dietary salecan (a water-soluble β-glucan) effectively reduces high-fat-diet-induced adiposity through disturbing bile-acid-promoted emulsification in mice. However, the effects of salecan on metabolic genes and metabolites involved in lipid accumulation are mostly unknown. Here, we confirmed that dietary 3% and 6% salecan for 4 weeks markedly decreased fat accumulation in liver and adipose tissue in high-fat-diet rats, displaying a decrease in mRNA levels of SREBP1-C, FAS, SCD1 and ACC1 involved in de novo lipogenesis and a reduction of levels of GPAT1, DGAT1 and DGAT2 related to triglyceride synthesis. Dietary salecan also increased the mRNA levels of PPARα and CYP7A1, which are related to fatty acid oxidation and cholesterol decomposition, respectively. In the Topics: Adipose Tissue, White; Adiposity; Animals; Anti-Obesity Agents; Antioxidants; beta-Glucans; Biomarkers; Cell Size; Diet, High-Fat; Dietary Supplements; Gene Expression Profiling; Gene Expression Regulation; Lipogenesis; Liver; Magnetic Resonance Spectroscopy; Male; Metabolomics; Non-alcoholic Fatty Liver Disease; Obesity; Oxidative Stress; Principal Component Analysis; Rats, Sprague-Dawley | 2017 |
Combination of β-glucan and Morus alba L. Leaf Extract Promotes Metabolic Benefits in Mice Fed a High-Fat Diet.
β-glucan (BG) and mulberry have received increasing attention for their benefits as natural sources of metabolic health. In the current study, we investigated the synergetic beneficial effects of BG and mulberry leaf extract (MLE) in mice fed a high-fat diet (HFD). Male C57BL6 mice were fed a HFD for twelve weeks to induce significant obesity and insulin resistance. BG and MLE were administrated orally throughout the feeding period. The administration of BG resulted in a significant reduction in body weight gain, perirenal fat mass, fasting insulin, serum lipids, serum inflammation markers, and fatty liver, showing systemic health improvement. Likewise, the administration of MLE showed benefits similar to BG, with the exception of body weight gain. In addition to the systemic benefits, the combination of BG and MLE resulted in a synergetic improvement in insulin sensitivity. Meanwhile, only the combination of BG and MLE significantly enhanced liver GST (Glutathione S-Transferase) activity and CuZn-SOD (Superoxide dismutase (Cu-Zn)) activity, resulting in a significant reduction in GSH/GSSG (Glutathione disulfide) and reactive oxygen species (ROS) levels in the liver. These results further confirm the beneficial effects of BG and MLE on metabolic disorders and show that the combination of BG and MLE has synergetic effects. Topics: Adiposity; Animals; Anti-Inflammatory Agents; Antioxidants; beta-Glucans; Biomarkers; Diet, High-Fat; Disease Models, Animal; Drug Synergism; Drug Therapy, Combination; Hypoglycemic Agents; Hypolipidemic Agents; Inflammation Mediators; Insulin; Insulin Resistance; Lipids; Liver; Male; Mice, Inbred C57BL; Morus; Non-alcoholic Fatty Liver Disease; Obesity; Oxidative Stress; Plant Extracts; Plant Leaves; Time Factors; Weight Gain | 2017 |
Oat β-glucan inhibits lipopolysaccharide-induced nonalcoholic steatohepatitis in mice.
Nonalcoholic steatohepatitis (NASH) is part of the spectrum of nonalcoholic fatty liver disease. However, there are few suitable animal models to study the pathogenesis of NASH or very limited advances in the prevention. Our aims were to establish a mouse model of NASH by intraperitoneally injecting lipopolysaccharide (LPS) at a dose of 1.5 mg per kg body weight per day for 6 weeks and to investigate the potential inhibitory effects of oat β-glucan (1%, 5%, or 10%) added to a specific pathogen-free diet. Intraperitoneal injection of LPS for 6 weeks increased serum LPS levels; decreased serum glucagon-like peptide-2 levels; triggered abnormal aminotransferase activity, glucose intolerance, and insulin resistance; and increased hepatic proinflammatory cytokines (tumor necrosis factor-α, interleukin-6, interleukin-1β), triglyceride, and malonyl dialdehyde levels; but reduced hepatic superoxide dismutase activity. Histologic evaluation revealed evidence of hepatic steatosis, inflammation, and mild necrosis in LPS-treated mice. Dietary supplementation of oat β-glucan prevented most of the LPS-induced metabolic disorders, and improved hepatic steatosis and inflammation, although a dose-dependent effect was not observed. In conclusion, oat β-glucan could inhibit LPS-induced NASH in mice. Topics: Animals; Avena; beta-Glucans; Disease Models, Animal; Dose-Response Relationship, Drug; Endotoxemia; Fatty Liver; Glucagon-Like Peptide 2; Glucose Intolerance; Inflammation; Insulin Resistance; Interleukin-1beta; Interleukin-6; Lipopolysaccharides; Liver; Male; Malondialdehyde; Mice; Mice, Inbred C57BL; Non-alcoholic Fatty Liver Disease; Oxidative Stress; Superoxide Dismutase; Transaminases; Triglycerides; Tumor Necrosis Factor-alpha; Weight Gain | 2013 |