{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,17]],"date-time":"2026-07-17T17:25:54Z","timestamp":1784309154162,"version":"3.55.0"},"reference-count":54,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2013,10,14]],"date-time":"2013-10-14T00:00:00Z","timestamp":1381708800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Liver International"],"published-print":{"date-parts":[[2014,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background &amp; Aims<\/jats:title><jats:p>Non\u2010alcoholic fatty liver disease (<jats:styled-content style=\"fixed-case\">NAFLD<\/jats:styled-content>) is associated with increased cardiovascular disease (<jats:styled-content style=\"fixed-case\">CVD<\/jats:styled-content>) risk. Non\u2010high\u2010density lipoprotein cholesterol (non\u2010<jats:styled-content style=\"fixed-case\">HDL<\/jats:styled-content>\u2010C), i.e. total cholesterol minus <jats:styled-content style=\"fixed-case\">HDL<\/jats:styled-content>, is a well\u2010established risk factor for <jats:styled-content style=\"fixed-case\">CVD<\/jats:styled-content>; however, its association with <jats:styled-content style=\"fixed-case\">NAFLD<\/jats:styled-content> development has not been established. Our aim was to test whether non\u2010<jats:styled-content style=\"fixed-case\">HDL<\/jats:styled-content>\u2010C is an independent predictor of new onset of <jats:styled-content style=\"fixed-case\">NAFLD<\/jats:styled-content>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>A prospective cohort study of 213 subjects from the general population, without liver disease, was studied. Evaluation of medical history, dietary and physical activity habits, fasting blood tests and ultrasonographic evidence of <jats:styled-content style=\"fixed-case\">NAFLD<\/jats:styled-content> was performed at baseline and after a 7\u2010year follow\u2010up by identical protocols.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>From 147 patients that did not have <jats:styled-content style=\"fixed-case\">NAFLD<\/jats:styled-content> at baseline, 28 (19%) developed <jats:styled-content style=\"fixed-case\">NAFLD<\/jats:styled-content> at the 7\u2010year follow\u2010up. The baseline levels of non\u2010<jats:styled-content style=\"fixed-case\">HDL<\/jats:styled-content>\u2010C were higher among subjects who developed <jats:styled-content style=\"fixed-case\">NAFLD<\/jats:styled-content> (179.5\u00a0\u00b1\u00a037.1 vs. 157.3\u00a0\u00b1\u00a035.1\u00a0mg\/dl, <jats:italic>P<\/jats:italic>\u00a0=\u00a00.003). Non\u2010<jats:styled-content style=\"fixed-case\">HDL<\/jats:styled-content>\u2010C independently predicted new onset of <jats:styled-content style=\"fixed-case\">NAFLD<\/jats:styled-content> adjusting for age, gender, <jats:styled-content style=\"fixed-case\">BMI<\/jats:styled-content> or waist circumference, lifestyle and serum insulin (<jats:styled-content style=\"fixed-case\">OR<\/jats:styled-content>\u00a0=\u00a01.02 for every mg\/dl increment, 1.01\u20131.04 95% <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>,<jats:italic> P<\/jats:italic>\u00a0=\u00a00.008). Non\u2010<jats:styled-content style=\"fixed-case\">HDL<\/jats:styled-content>\u2010C was a stronger predictor for <jats:styled-content style=\"fixed-case\">NAFLD<\/jats:styled-content> than total cholesterol, low\u2010density lipoprotein cholesterol, triglycerides and <jats:styled-content style=\"fixed-case\">HDL<\/jats:styled-content>. No patients with non\u2010<jats:styled-content style=\"fixed-case\">HDL<\/jats:styled-content>\u2010C\u00a0&lt;\u00a0130\u00a0mg\/dl developed <jats:styled-content style=\"fixed-case\">NAFLD<\/jats:styled-content>, whereas 20.8% of those with values between 130 to 160 and 24.6% of those with values &gt;160\u00a0mg\/dl developed <jats:styled-content style=\"fixed-case\">NAFLD<\/jats:styled-content> (<jats:italic>P<\/jats:italic> for trend\u00a0= 0.015).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Non\u2010<jats:styled-content style=\"fixed-case\">HDL<\/jats:styled-content>\u2010C is an independent predictor for <jats:styled-content style=\"fixed-case\">NAFLD<\/jats:styled-content> and a stronger predictor than other lipoproteins. This association may stem from the combined hepato\u2010toxic effect of non\u2010<jats:styled-content style=\"fixed-case\">HDL<\/jats:styled-content>\u2010C and may explain the association between <jats:styled-content style=\"fixed-case\">NAFLD<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">CVD<\/jats:styled-content>.<\/jats:p><\/jats:sec>","DOI":"10.1111\/liv.12318","type":"journal-article","created":{"date-parts":[[2013,9,11]],"date-time":"2013-09-11T11:51:15Z","timestamp":1378900275000},"source":"Crossref","is-referenced-by-count":63,"title":["Non\u2010high\u2010density lipoprotein cholesterol independently predicts new onset of non\u2010alcoholic fatty liver disease"],"prefix":"10.1111","volume":"34","author":[{"given":"Shira","family":"Zelber\u2010Sagi","sequence":"first","affiliation":[{"name":"Department Gastroenterology Tel\u2010Aviv Medical Center Tel\u2010Aviv Israel"},{"name":"School of Public Health Faculty of Social Welfare and Health Sciences 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