Nonalcoholic steatohepatitis, insulin resistance, and metabolic syndrome: Further evidence for an etiologic association

摘要: This study aims to determine the presence of components metabolic syndrome in primary nonalcoholic steatohepatitis (NASH) and assess role liver disease genesis peripheral hyperinsulinemia. Nineteen patients (18 men 1 woman; mean age, +/- SD, 38 10 years; body mass index [BMI], 26 2 kg/m(2)) with histologic evidence NASH were enrolled; 19 age- sex-matched normal subjects investigated as controls. Plasma glucose, insulin, C-peptide levels measured during an oral glucose tolerance test, a frequently sampled intravenous test (FSIGT), analyzed by minimal modeling technique, was performed. Compared controls, group had lower insulin sensitivity (3.84 2.44 vs. 7.48 3.01 10(-4) x min(-1)/microU/mL; P =.0003) higher total secretion (21 13 3 nmol/L 240 minutes; =.001). Hepatic extraction similar both groups (69.8% 16.1% 70.2% 18.3%; =.854). According results no patient classified diabetic, 5 intolerant, having impaired fasting glycemia. Nine (47%) at least minimum criteria required define according European Group for Study Insulin Resistance (EGIR). In conclusion, hyperinsulinemia resistance occur NASH; these conditions do not stem from reduced hepatic but enhanced pancreatic compensatory sensitivity. The derangement regulation, often associated syndrome, may play causal pathogenesis NASH.