Relation of hepatic steatosis to atherogenic dyslipidemia

Hepatic steatosis is closely associated with the metabolic syndrome. We assessed for an independent association between hepatic steatosis and atherogenic dyslipidemia after adjustment for obesity, physical activity, hyperglycemia, and systemic inflammation. We studied 6,333 asymptomatic subjects without clinical cardiovascular disease undergoing a health screen in Brazil from November 2008 to July 2010. Hepatic steatosis was diagnosed by ultrasound. Atherogenic dyslipidemia was defined using 2 definitions: criteria for (1) metabolic syndrome or (2) insulin resistance (triglyceride/high-density-lipoprotein cholesterol ratio of ≥2.5 in women and ≥3.5 in men). In hierarchical multivariate regression models, we evaluated for an independent association of hepatic steatosis with atherogenic dyslipidemia. Hepatic steatosis was detected in 36% of participants (average age 43.5 years, 79% men, average body mass index 26.3 kg/m(2)). Subjects with hepatic steatosis had similar levels of low-density-lipoprotein cholesterol, with significantly lower level of high-density-lipoprotein cholesterol and higher level of triglyceride compared with those without steatosis. Hepatic steatosis remained significantly independently associated with atherogenic dyslipidemia of both definitions (metabolic syndrome [odds ratio 2.47, 95% confidence interval 2.03 to 3.02] and insulin resistance [odds ratio 2.50, 95% confidence interval 2.13 to 2.91]) after multivariate adjustment. Stratified analyses showed a persistent independent association in nonobese subjects, those without metabolic syndrome, those with normal high-sensitivity C-reactive protein, nonalcohol abusers, and those with normal liver enzymes. Hepatic steatosis was significantly associated with atherogenic dyslipidemia independent of obesity, physical activity, hyperglycemia, and systemic inflammation after multivariate adjustment. In conclusion, this adds to the growing body of evidence that hepatic steatosis may play a direct metabolic role in conferring increased cardiovascular risk.