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However, only a few prospective studies evaluated <jats:styled-content style=\"fixed-case\">NAFLD<\/jats:styled-content> as a predictor for <jats:styled-content style=\"fixed-case\">DM<\/jats:styled-content>, most did not adjust for the full range of potential cofounders and none used an objectively quantified degree of steatosis. Our aim was to evaluate the independent role of <jats:styled-content style=\"fixed-case\">NAFLD<\/jats:styled-content> in predicting the development of pre\u2010<jats:styled-content style=\"fixed-case\">DM<\/jats:styled-content> in a 7\u2010year prospective follow\u2010up of healthy volunteers.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>A prospective cohort of a subsample of the Israeli National Health Survey evaluated at baseline and after 7\u00a0years by identical protocols. Metabolic parameters and ultrasonographic evidence of <jats:styled-content style=\"fixed-case\">NAFLD<\/jats:styled-content> were evaluated in 213 subjects, without known liver disease or history of alcohol abuse. Exclusion criteria were pre\u2010<jats:styled-content style=\"fixed-case\">DM<\/jats:styled-content> at the baseline survey. Steatosis was quantified by ultrasound with the hepato\u2010renal ultrasound index (<jats:styled-content style=\"fixed-case\">HRI<\/jats:styled-content>).<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The study included 141 volunteers (mean age 48.78\u00a0\u00b1\u00a09.68, 24.82% with <jats:styled-content style=\"fixed-case\">NAFLD<\/jats:styled-content>) without pre\u2010<jats:styled-content style=\"fixed-case\">DM<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">DM<\/jats:styled-content> at baseline. Both <jats:styled-content style=\"fixed-case\">NAFLD<\/jats:styled-content> on regular <jats:styled-content style=\"fixed-case\">US<\/jats:styled-content> (<jats:styled-content style=\"fixed-case\">OR<\/jats:styled-content>=2.93, 1.02\u20138.41 95%<jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>) and <jats:styled-content style=\"fixed-case\">HRI<\/jats:styled-content> (<jats:styled-content style=\"fixed-case\">OR<\/jats:styled-content>=7.87, 1.83\u201333.82) were independent predictors for the development of pre\u2010<jats:styled-content style=\"fixed-case\">DM<\/jats:styled-content>, adjusting for age, gender, <jats:styled-content style=\"fixed-case\">BMI<\/jats:styled-content>, family history of <jats:styled-content style=\"fixed-case\">DM<\/jats:styled-content>, baseline insulin, adiponectin and glucose. Further adjustment for physical activity and dietary intake did not weaken the association. Furthermore, <jats:styled-content style=\"fixed-case\">NAFLD<\/jats:styled-content> was a stronger predictor for pre\u2010<jats:styled-content style=\"fixed-case\">DM<\/jats:styled-content> than the metabolic syndrome. Subjects with both <jats:styled-content style=\"fixed-case\">NAFLD<\/jats:styled-content> and glucose \u226589 had 93.3% incidence rate of pre\u2010<jats:styled-content style=\"fixed-case\">DM<\/jats:styled-content>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Non\u2010alcoholic fatty liver disease is a strong and independent risk factor for pre\u2010<jats:styled-content style=\"fixed-case\">DM<\/jats:styled-content> in the general adult population; thus, <jats:styled-content style=\"fixed-case\">NAFLD<\/jats:styled-content> patients should be classified as a population at risk.<\/jats:p><\/jats:sec>","DOI":"10.1111\/liv.12200","type":"journal-article","created":{"date-parts":[[2013,4,19]],"date-time":"2013-04-19T09:43:23Z","timestamp":1366364603000},"page":"1406-1412","source":"Crossref","is-referenced-by-count":76,"title":["Non\u2010alcoholic fatty liver disease independently predicts prediabetes during a 7\u2010year prospective 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