title: Insights from Genome-Wide Association Analyses of Nonalcoholic Fatty Liver Disease.
abstract: 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. Nonalcoholic fatty liver disease will become the number one cause of liver disease worldwide by 2020. Nonalcoholic fatty liver disease is correlated albeit imperfectly with obesity and other metabolic diseases such as diabetes, hyperlipidemia, and cardiovascular disease, but exactly how having one of these diseases contributes to the development of other metabolic diseases is only now being elucidated. Development of NAFLD and related metabolic diseases is genetically influenced in the population, and recent genome-wide association studies (GWASs) have discovered genetic variants that associate with these diseases. These GWAS-associated variants cannot only help us to identify individuals at high risk of developing NAFLD, but also to better understand its pathophysiology so that we can develop more effective treatments for this disease and related metabolic diseases in the future.
authors.affiliation: Division of Gastroenterology, Department of Internal Medicine, Department of Computational Medicine and Bioinformatics, University of Michigan, Ann Arbor, Michigan.
authors.forename: Bratati
authors.initials: B
authors.lastname: Kahali
authors.affiliation: Division of Gastroenterology, Department of Internal Medicine, Department of Computational Medicine and Bioinformatics, University of Michigan, Ann Arbor, Michigan.
authors.forename: Brian
authors.initials: B
authors.lastname: Halligan
authors.affiliation: Division of Gastroenterology, Department of Internal Medicine, Department of Computational Medicine and Bioinformatics, University of Michigan, Ann Arbor, Michigan.
authors.forename: Elizabeth K
authors.initials: EK
authors.lastname: Speliotes
mesh_terms: D048868:Adaptor Proteins, Signal Transducing / Q000235:genetics; D006528:Carcinoma, Hepatocellular / Q000235:genetics* / Q000601:surgery; D020022:Genetic Predisposition to Disease; D055106:Genome-Wide Association Study; D006084:Graft Rejection / Q000235:genetics; D006085:Graft Survival / Q000235:genetics; D006801:Humans; D007333:Insulin Resistance / Q000235:genetics; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics; D008049:Lipase / Q000235:genetics; D008113:Liver Neoplasms / Q000235:genetics* / Q000601:surgery; D016031:Liver Transplantation; D008245:Lysophospholipase / Q000235:genetics; D008565:Membrane Proteins / Q000235:genetics; D065626:Non-alcoholic Fatty Liver Disease / Q000235:genetics* / Q000378:metabolism / Q000601:surgery; D009765:Obesity / Q000235:genetics / Q000378:metabolism; D011110:Polymorphism, Genetic; D054645:Protein Phosphatase 1 / Q000235:genetics; D017346:Protein Serine-Threonine Kinases / Q000037:antagonists & inhibitors / Q000235:genetics; D000217:Acyltransferases; D054512:Phospholipases A2, Calcium-Independent
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D047908:Intracellular Signaling Peptides and Proteins; D008049:Lipase; D008245:Lysophospholipase; D008565:Membrane Proteins; D054645:Protein Phosphatase 1; D017346:Protein Serine-Threonine Kinases; C485100:GCKR protein, human; C419195:TM6SF2 protein, human; C493170:TRIB1 protein, human; C533682:PNPLA3 protein, human; D000217:Acyltransferases; D054512:Phospholipases A2, Calcium-Independent; C561408:LYPLAL1 protein, human; C586823:PPP1R3B protein, human