Background: Animal studies have suggested that adiponec- tin may play a role in the pathogenesis of alcoholic and nonalcoholic fatty li ver disease. Studies are limited that evaluated the role of adiponectin in the p athogenesis of nonalcoholic steatohepatitis(NASH). Methods: To further our under standing of the role of adiponectin in the pathogenesis of NASH, the following s tudies were conducted. Serum adiponectin was measured and correlated with anthro pometric and nutritional variables in 21 patients with biopsy-proven NASH and 1 9 age-, gender-,body mass index-, and body fat-matched controls. The effect of a mixed meal on serum adiponectin levels in a subgroup of patients (n = 24) w ith NASH and controls was assessed. In a separate cohort, liver samples belonging to healthy (n= 11), steatotic (n = 12), and NASH (n = 12) patients were used to further explore the role of adip onectin by measuring the expression of adiponectin and adiponectin receptor (Adi poR2)mRNA. Results: Patients with NASH had significantly lower levels of serum a diponectin than controls (4.9 ±2.7 vs.7.3 ±3.5 μg/mL, P = 0.02). While no sig nificant correlation existed between serum adiponectin and anthropometric or nut ritional variables, it was independently associated with age,high density lipopr otein, and triglycerides. Mixed meal had no effect on serum adiponectin either i n patients with NASH or in controls. There was no expression of adiponectin mRNA in any of liver samples studied. However, AdipoR2 mRNA expression was higher in NASH than in steatotic and normal liver tissue. Conclusion: These data show tha t adiponectin may have a role in the pathogenesis of human NASH investigated fur ther. Background: Animal studies have suggested that adiponec-tin may play a role in the pathogenesis of alcoholic and nonalcoholic fatty li ver disease. Studies are limited that evaluated as role of adiponectin in the p athogenesis of nonalcoholic steatohepatitis (NASH). Methods: To further our under standing of the role of adiponectin in the pathogenesis of NASH, the following s tudies were conducted. Serum adiponectin was measured and correlated with anthropometric and nutritional variables in 21 patients with biopsy-proven NASH and 1 9 age-, gender-, body mass index-, and body fat-matched controls. The effect of a mixed meal on serum adiponectin levels in a subgroup of patients (n = 24) w ith NASH and controls was assessed. In a separate cohort, liver samples belonging to healthy (n = 12), and NASH (n = 12) patients were used to further explore the role of adiponectin by measuring the expression of adiponectin and adiponectin receptor (Adi poR2) mRNA. Results: Patient s with NASH had significantly lower levels of serum a diponectin than controls (4.9 ± 2.7 vs.7.3 ± 3.5 μg / mL, P = 0.02). While no sig nificant correlation existed between serum adiponectin and anthropometric or nutraition variables, it was independent associated with age, high density lipoprotein, and triglycerides. There was no expression of adiponectin mRNA in any of liver samples studied. However, AdipoR2 mRNA expression was higher in NASH than in steatotic and normal liver tissue. Conclusion: These data show tha t adiponectin may have a role in the pathogenesis of human NASH investigated fur ther.