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Background/Aims: There is increasing interest in the influence of excess body weight and associated metabolic factors on the liver. In patients with non-alcoholic steatohepatitis, lower levels of adiponectin were associated with higher g rades of hepatic steatosis and necroinflammatory activity, suggesting a pathophysiological role for this adipokine in liver disease. Methods: We studied 194 consecutive patients with untreated chronic HCV, t o assess the relationship between adiponectin and its receptors and hepatic stea tosis, fibrosis and inflammation. Results: Significant negative correlations bet ween serum adiponectin and male gender, body mass index and serum insulin were o bserved. However, there was no association between serum adiponectin and stage o f fibrosis and lower levels of serum adiponectin were associated with the presen ce of steatosis in males only. In contrast, there was a significant increase in serum adiponectin and hepatic adiponectin immunoreactivity with increasing infla mmation. The hepatic mRNA expression of the adiponectin receptors, AdipoR1 and A dipoR2, displayed significant but opposite associations with phosphoenolpyruvate carboxykinase (PEPCK) gene expression, a substitute marker of hepatic insulin s ensitivity. Conclusions: In patients with chronic HCV, adiponectin was associate d with steatosis only in males and was paradoxically increased with inflammation . Our results suggest that the role of adiponectin in chronic liver diseases may be linked to gender and etiology.
Background / Aims: There is increasing interest in the influence of excess body weight and associated metabolic factors on the liver. In patients with non-alcoholic steatohepatitis, lower levels of adiponectin were associated with higher g rades of hepatic steatosis and necroinflammatory activity, suggesting a pathophysiological role for this adipokine in liver disease. Methods: We studied 194 consecutive patients with untreated chronic HCV, to assess the relationship between adiponectin and its receptors and hepatic stea tosis, fibrosis and inflammation. Results: Significant negative correlations bet ween serum adiponectin and male Gender, body mass index and serum insulin were o bserved. However, there was no association between serum adiponectin and stage of fibrosis and lower levels of serum adiponectin were associated with the presen ce of steatosis in males only. In contrast, there was a significant increase in serum adiponectin and hepatic adiponectin immunoreactivity with incre asing infla mmation. The hepatic mRNA expression of the adiponectin receptors, AdipoR1 and A dipoR2, displayed significant but vice associations with phosphoenolpyruvate carboxykinase (PEPCK) gene expression, a substitute marker of hepatic insulin s ensitivity. Conclusions: In patients with chronic HCV, adiponectin was associate d with steatosis only in males and was paradoxically increased with inflammation. Our results suggest that the role of adiponectin in chronic liver diseases may be linked to gender and etiology.