nicotinamide-beta-riboside and Fatty-Liver

nicotinamide-beta-riboside has been researched along with Fatty-Liver* in 2 studies

Other Studies

2 other study(ies) available for nicotinamide-beta-riboside and Fatty-Liver

Article	Year
Overexpression of NRK1 ameliorates diet- and age-induced hepatic steatosis and insulin resistance. Biochemical and biophysical research communications, 2018, 06-02, Volume: 500, Issue:2 NAD Topics: Aging; Animals; Diet, High-Fat; Fatty Liver; HEK293 Cells; Humans; Insulin Resistance; Lipid Metabolism; Liver; Male; Mice; Mice, Inbred C57BL; NAD; Niacinamide; NIH 3T3 Cells; Phosphotransferases (Alcohol Group Acceptor); Pyridinium Compounds; Triglycerides	2018
Eliciting the mitochondrial unfolded protein response by nicotinamide adenine dinucleotide repletion reverses fatty liver disease in mice. Hepatology (Baltimore, Md.), 2016, Volume: 63, Issue:4 With no approved pharmacological treatment, nonalcoholic fatty liver disease (NAFLD) is now the most common cause of chronic liver disease in Western countries and its worldwide prevalence continues to increase along with the growing obesity epidemic. Here, we show that a high-fat high-sucrose (HFHS) diet, eliciting chronic hepatosteatosis resembling human fatty liver, lowers hepatic nicotinamide adenine dinucleotide (NAD(+) ) levels driving reductions in hepatic mitochondrial content, function, and adenosine triphosphate (ATP) levels, in conjunction with robust increases in hepatic weight, lipid content, and peroxidation in C57BL/6J mice. To assess the effect of NAD(+) repletion on the development of steatosis in mice, nicotinamide riboside, a precursor of NAD(+) biosynthesis, was added to the HFHS diet, either as a preventive strategy or as a therapeutic intervention. We demonstrate that NR prevents and reverts NAFLD by inducing a sirtuin (SIRT)1- and SIRT3-dependent mitochondrial unfolded protein response, triggering an adaptive mitohormetic pathway to increase hepatic β-oxidation and mitochondrial complex content and activity. The cell-autonomous beneficial component of NR treatment was revealed in liver-specific Sirt1 knockout mice (Sirt1(hep-/-) ), whereas apolipoprotein E-deficient mice (Apoe(-/-) ) challenged with a high-fat high-cholesterol diet affirmed the use of NR in other independent models of NAFLD.. Our data warrant the future evaluation of NAD(+) boosting strategies to manage the development or progression of NAFLD. Topics: Analysis of Variance; Animals; Area Under Curve; Biopsy, Needle; Diet, High-Fat; Disease Models, Animal; Fatty Liver; Immunohistochemistry; Lipid Metabolism; Male; Mice; Mice, Inbred C57BL; Mitochondria; NAD; Niacinamide; Pyridinium Compounds; Random Allocation; Sensitivity and Specificity; Treatment Outcome; Unfolded Protein Response	2016

Article

Year

Overexpression of NRK1 ameliorates diet- and age-induced hepatic steatosis and insulin resistance.

Biochemical and biophysical research communications, 2018, 06-02, Volume: 500, Issue:2

NAD

Topics: Aging; Animals; Diet, High-Fat; Fatty Liver; HEK293 Cells; Humans; Insulin Resistance; Lipid Metabolism; Liver; Male; Mice; Mice, Inbred C57BL; NAD; Niacinamide; NIH 3T3 Cells; Phosphotransferases (Alcohol Group Acceptor); Pyridinium Compounds; Triglycerides

2018

Eliciting the mitochondrial unfolded protein response by nicotinamide adenine dinucleotide repletion reverses fatty liver disease in mice.

Hepatology (Baltimore, Md.), 2016, Volume: 63, Issue:4

With no approved pharmacological treatment, nonalcoholic fatty liver disease (NAFLD) is now the most common cause of chronic liver disease in Western countries and its worldwide prevalence continues to increase along with the growing obesity epidemic. Here, we show that a high-fat high-sucrose (HFHS) diet, eliciting chronic hepatosteatosis resembling human fatty liver, lowers hepatic nicotinamide adenine dinucleotide (NAD(+) ) levels driving reductions in hepatic mitochondrial content, function, and adenosine triphosphate (ATP) levels, in conjunction with robust increases in hepatic weight, lipid content, and peroxidation in C57BL/6J mice. To assess the effect of NAD(+) repletion on the development of steatosis in mice, nicotinamide riboside, a precursor of NAD(+) biosynthesis, was added to the HFHS diet, either as a preventive strategy or as a therapeutic intervention. We demonstrate that NR prevents and reverts NAFLD by inducing a sirtuin (SIRT)1- and SIRT3-dependent mitochondrial unfolded protein response, triggering an adaptive mitohormetic pathway to increase hepatic β-oxidation and mitochondrial complex content and activity. The cell-autonomous beneficial component of NR treatment was revealed in liver-specific Sirt1 knockout mice (Sirt1(hep-/-) ), whereas apolipoprotein E-deficient mice (Apoe(-/-) ) challenged with a high-fat high-cholesterol diet affirmed the use of NR in other independent models of NAFLD.. Our data warrant the future evaluation of NAD(+) boosting strategies to manage the development or progression of NAFLD.

Topics: Analysis of Variance; Animals; Area Under Curve; Biopsy, Needle; Diet, High-Fat; Disease Models, Animal; Fatty Liver; Immunohistochemistry; Lipid Metabolism; Male; Mice; Mice, Inbred C57BL; Mitochondria; NAD; Niacinamide; Pyridinium Compounds; Random Allocation; Sensitivity and Specificity; Treatment Outcome; Unfolded Protein Response

2016