Obesity increases the susceptibility to harbor AITD with an emerging role for leptin as a peripheral determinant, which needs to be confirmed in future investigations.

OBJECTIVE: The aim of this study was to evaluate liver steatosis in prepubertal and pubertal obese and the correlations with the lipid pro®le, the serum levels of hepatic parameters and the glycemic and insulinemic responses to an oral glucose tolerance test. SUBJECTS: 375 obese, 205 males and 170 females, Tanner pubertal stage I (n 82), stages II ± III (n 80) and stages IV ± V (n 213). MEASUREMENTS: Body mass index (BMI), waist ± hip ratio (WHR), total cholesterol and high density lipoprotein (HDL), cholesterolaHDL ratio, low density lipoprotein (LDL), very low density lipoprotein (VLDL), triglycerides (TGL), aspartate aminotransferase (AST), alanine aminotransferase (ALT), gGT, glycemia (G), insulinemia (IRI), fasting IRIaG ratio (FIGR), glycemic (mean blood glucose, MBG) and insulinemic (mean serum insulin, MSI) responses during a 120 min oral glucose tolerance test (OGTT), expressed as area under the curve (AUC)a120 min, pancreatic insulinemic response to glucose (IRG), and liver ultrasound scanning for assessing the degree of steatosis (moderate, severe). RESULTS: Liver steatosis was found in 33% of subjects in Tanner pubertal stage I, 36% in stage II ± III and 47% in stages IV ± V. BMI and transaminases were correlated with the degree of steatosis in all pubertal stages. AST, ALT and gGT were higher in the presence of steatosis, while elevated TGL was present in late puberty only; however the increase of ALT is speci®c for steatosis. CONCLUSION: Juvenile obesity involves a high risk of liver steatosis associated with alterations of transaminases and lipid but not glucose metabolism. These changes are apparent even to the prepubertal stage.