Gender-Specific Prevalences of Fatty Liver in Obese Children and Adolescents: Roles of Body Fat Distribution, Sex Steroids, and Insulin Resistance

Context: Nonalcoholic fatty liver disease (NAFLD) is known to have a gender-dimorphic prevalence in obese children. Less information is available on predictive factors for NAFLD in obese youths. Objective: The aim of the study was to examine the prevalence pattern and to identify clinical and laboratory markers associated with the risk for NAFLD. Design: This was a cross-sectional study. Setting: The study setting was a rehabilitation clinic. Study Participants: A total of 532 obese subjects (291 girls) aged 8-19 yr participated in the study. Main Measurements: Steatosis hepatis and visceral fat mass were determined by ultrasound. Laboratory tests included serum lipids, adiponectin, high-sensitivity C-reactive protein, sex steroids, and an oral glucose tolerance test. Results: Prevalence of hepatic steatosis was significantly higher in boys (41.1%) than in girls (17.2%) and was highest in postpubertal boys (51.2%) and lowest in postpubertal girls (12.2%). Severity of steatosis was associated with increased visceral fat mass, insulin resistance, lower adiponectin levels, and higher blood pressure. Three factors were extracted from the panel of investigated parameters by principal component analysis. Logistic regression analysis revealed significant associations of simple steatosis with the "insulin resistance and visceral fat" factor and the "body fat distribution and inflammation" factor in both genders and additionally with the "steroid hormones" factor in girls. Risk for steatosis hepatis with concomitantly elevated ALT was associated only with "insulin resistance and visceral fat" in girls and with all three factors in boys. Conclusion: Our results suggest significant associations of NAFLD with markers of visceral obesity and insulin resistance in both genders and gender-specific associations with parameters of body fat distribution and sex steroids. (J Clin Endocrinol Metab 94: 3872-3881, 2009)