title: Fatty Acid and Glucose Sensors in Hepatic Lipid Metabolism: Implications in NAFLD.
abstract: The term nonalcoholic fatty liver disease (NAFLD) covers a pathologic spectrum from lipid accumulation alone (simple steatosis) to steatosis with associated inflammation and fibrosis (nonalcoholic steatohepatitis [NASH]). Nonalcoholic steatohepatitis can progress to cirrhosis and potentially to hepatocellular carcinoma. Although a genetic predisposition has been highlighted, NAFLD is strongly associated with an unhealthy lifestyle and hypercaloric diet in the context of obesity and metabolic disease. The dysregulation of specific pathways (insulin signaling, mitochondrial function, fatty acid, and lipoprotein metabolism) have been linked to steatosis, but elucidating the molecular events determining evolution of the disease still requires further research before it can be translated into specific personalized interventional strategies. In this review, the authors focus on the early events of the pathophysiology of NASH, dissecting the metabolic and nutritional pathways involving fatty acids and glucose sensors that can modulate lipid accumulation in the liver, but also condition the progression to cirrhosis and hepatocellular carcinoma.
authors.affiliation: Medical Research Council - Human Nutrition Research (MRC-HNR), Cambridge, United Kingdom.
authors.forename: Michele
authors.initials: M
authors.lastname: Vacca
authors.affiliation: Liver Unit, Department of Medicine, Cambridge Biomedical Research Centre, Cambridge University NHS Foundation Trust, United Kingdom.
authors.forename: Michael
authors.initials: M
authors.lastname: Allison
authors.affiliation: Medical Research Council - Human Nutrition Research (MRC-HNR), Cambridge, United Kingdom.
authors.forename: Julian L
authors.initials: JL
authors.lastname: Griffin
authors.affiliation: Department of Clinical Biochemistry and University of Cambridge Metabolic Research Laboratories, Institute of Metabolic Science, Cambridge, United Kingdom.
authors.forename: Antonio
authors.initials: A
authors.lastname: Vidal-Puig
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism / Q000503:physiopathology; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D018450:Disease Progression; D005227:Fatty Acids / Q000097:blood / Q000378:metabolism*; D006801:Humans; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D008099:Liver / Q000378:metabolism* / Q000503:physiopathology; D008930:Mitochondria, Liver / Q000378:metabolism; D065626:Non-alcoholic Fatty Liver Disease / Q000097:blood / Q000175:diagnosis / Q000378:metabolism* / Q000503:physiopathology; D011379:Prognosis; D012307:Risk Factors
chemical_list: D001786:Blood Glucose; D005227:Fatty Acids; D007328:Insulin