Esteatosis hepática, resistencia a la insulina y adiponectina en una población con obesidad

Abstract

Introduction To study the clinical and laboratory relationships of fatty liver disease in a group of obese children and to investigate whether circulating adiponectin is related to fatty liver disease. Patients and methods Two hundred-ninety obese patients (age 4–18 years) were studied. Baseline body mass index-standard deviation score (BMI-SDS), acanthosis nigricans, blood pressure, plasma lipids, uric acid, alanine aminotransferase (ALT) and adiponectin were assessed, and a standard oral glucose tolerance test was performed. Insulin resistance (RI) was estimated by the homeostasis model assessment (HOMA) and liver steatosis was assessed by ultrasound (US). Children were classified as having metabolic syndrome if they met three or more of the following criteria: obesity, hypertension, hypertriglyceridemia, low HDL-cholesterol and impaired glucose metabolism. Results Fifty-two subjects (18%) had fatty liver by US and 22 (8%) had elevated ALT levels (≥40 U/L). Subjects with steatosis were significantly older (12.2±2.4 frente a 11.1±2.9 yr), heavier (BMI-SDS: 4.5±1.5 frente a 3.8±1.3), and more RI (HOMA: 3.7±1.5 frente a 2.4±1.4), but were comparable in gender, pubertal status and racial distribution to those with normal US. The prevalence of metabolic syndrome and acanthosis nigricans were also higher in the steatosis frente a the normal US group. Serum adiponectin concentration was inversely correlated with age, HOMA, ALT and uric acid and directly correlated with HDL-cholesterol. In a multiple logistic regression analysis, BMI-SDS, HOMA and serum adiponectin, but not age, uric acid or triglycerides, were the covariates independently associated with the presence of steatosis (odds ratio 1.4 [1.1-1.9]; 1.3 [1.1-1.6] and 0.9 [0.8-0.9], respectively). Conclusions Obesity and RI are risk factors for liver steatosis in children and adolescents. Decreased serum adiponectin is closely and independently associated with steatosis.