{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T13:31:31Z","timestamp":1790775091022,"version":"4.1.0"},"reference-count":45,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"7","license":[{"start":{"date-parts":[[2019,4,18]],"date-time":"2019-04-18T00:00:00Z","timestamp":1555545600000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Hepatol Commun"],"published-print":{"date-parts":[[2019,7]]},"abstract":"<jats:p>The accumulation of excess fat in the liver (hepatic steatosis) in the absence of heavy alcohol consumption causes nonalcoholic fatty liver disease (NAFLD), which has become a global epidemic. Identifying metabolic risk factors that interact with the genetic risk of NAFLD is important for reducing disease burden. We tested whether serum glucose, insulin, insulin resistance, triglyceride (TG), low\u2010density lipoprotein cholesterol, high\u2010density lipoprotein cholesterol, body mass index (BMI), and waist\u2010to\u2010hip ratio adjusted for BMI interact with genetic variants in or near the patatin\u2010like phospholipase domain containing 3 (<jats:italic toggle=\"yes\">PNPLA3<\/jats:italic>) gene, the glucokinase regulatory protein (<jats:italic toggle=\"yes\">GCKR<\/jats:italic>) gene, the neurocan\/transmembrane 6 superfamily member 2 (<jats:italic toggle=\"yes\">NCAN\/TM6SF2<\/jats:italic>) gene<jats:italic toggle=\"yes\">,<\/jats:italic> and the lysophospholipase\u2010like 1 (<jats:italic toggle=\"yes\">LYPLAL1<\/jats:italic>) gene to exacerbate hepatic steatosis, estimated by liver attenuation. We performed association analyses in 10 population\u2010based cohorts separately and then meta\u2010analyzed results in up to 14,751 individuals (11,870 of European ancestry and 2,881 of African ancestry). We found that <jats:italic toggle=\"yes\">PNPLA3\u2010<\/jats:italic>rs738409 significantly interacted with insulin, insulin resistance, BMI, glucose, and TG to increase hepatic steatosis in nondiabetic individuals carrying the G allele. Additionally, <jats:italic toggle=\"yes\">GCKR\u2010<\/jats:italic>rs780094 significantly interacted with insulin, insulin resistance, and TG. Conditional analyses using the two largest European ancestry cohorts in the study showed that insulin levels accounted for most of the interaction of <jats:italic toggle=\"yes\">PNPLA3\u2010<\/jats:italic>rs738409 with BMI, glucose, and TG in nondiabetic individuals. Insulin, <jats:italic toggle=\"yes\">PNPLA3<\/jats:italic>\u2010rs738409, and their interaction accounted for at least 8% of the variance in hepatic steatosis in these two cohorts. <jats:italic toggle=\"yes\">Conclusion:<\/jats:italic> Insulin resistance, either directly or through the resultant elevated insulin levels, more than other metabolic traits, appears to amplify the <jats:italic toggle=\"yes\">PNPLA3<\/jats:italic>\u2010rs738409\u2010G genetic risk for hepatic steatosis. Improving insulin resistance in nondiabetic individuals carrying <jats:italic toggle=\"yes\">PNPLA3\u2010<\/jats:italic>rs738409\u2010G may preferentially decrease hepatic steatosis.<\/jats:p>","DOI":"10.1002\/hep4.1353","type":"journal-article","created":{"date-parts":[[2019,4,18]],"date-time":"2019-04-18T12:25:21Z","timestamp":1555590321000},"page":"894-907","source":"Crossref","is-referenced-by-count":55,"title":["Insulin Resistance Exacerbates Genetic Predisposition to Nonalcoholic Fatty Liver Disease in Individuals Without Diabetes"],"prefix":"10.1097","volume":"3","author":[{"given":"Llilda","family":"Barata","sequence":"first","affiliation":[{"name":"Division of Statistical Genomics, Department of Genetics,Washington University School of Medicine,St. Louis,MO"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mary F.","family":"Feitosa","sequence":"additional","affiliation":[{"name":"Division of Statistical Genomics, Department of Genetics,Washington University School of Medicine,St. Louis,MO"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lawrence F.","family":"Bielak","sequence":"additional","affiliation":[{"name":"Department of Epidemiology, School of Public Health,University of Michigan,Ann Arbor,MI"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brian","family":"Halligan","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology, Department of Internal Medicine, Department of Computational Medicine and Bioinformatics,University of Michigan,Ann Arbor,MI"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Abigail S.","family":"Baldridge","sequence":"additional","affiliation":[{"name":"Department of Preventive Medicine,Northwestern University Feinberg School of Medicine,Chicago,IL"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiuqing","family":"Guo","sequence":"additional","affiliation":[{"name":"Institute for Translational Genomics and Population Sciences, LABioMed and the Department of Pediatrics,Harbor\u2010University of California Los Angeles Medical Center,Torrance,CA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Laura M.","family":"Yerges\u2010Armstrong","sequence":"additional","affiliation":[{"name":"Department of Medicine,University of Maryland School of Medicine,Baltimore,MD"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Albert V.","family":"Smith","sequence":"additional","affiliation":[{"name":"Department of Biostatistics, School of Public Health,University of Michigan,Ann Arbor,MI"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jie","family":"Yao","sequence":"additional","affiliation":[{"name":"Institute for Translational Genomics and Population Sciences, LABioMed and the Department of Pediatrics,Harbor\u2010University of California Los Angeles Medical Center,Torrance,CA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicholette D.","family":"Palmer","sequence":"additional","affiliation":[{"name":"Department of Biochemistry,Wake Forest School of Medicine,Winston\u2010Salem,NC"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6264-2573","authenticated-orcid":false,"given":"Lisa B.","family":"VanWagner","sequence":"additional","affiliation":[{"name":"Department of Preventive Medicine,Northwestern University Feinberg School of Medicine,Chicago,IL"},{"name":"Division of Gastroenterology and Hepatology,Northwestern University Feinberg School of Medicine,Chicago,IL"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. 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