Hepatic steatosis and insulin resistance are associated with serum imbalance of adiponectin/tumour necrosis factor-alpha in chronic hepatitis C patients

Aliment Pharmacol Ther. 2006 Nov 1;24(9):1349-57. doi: 10.1111/j.1365-2036.2006.03114.x.

Abstract

Background: Steatosis and insulin resistance (IR) have a pathogenic role in chronic hepatitis C (HCV). Adipocytokines balance modulates hepatic lipid content and IR.

Aim: To evaluate serum adipocytokines and relationship with virological, histological and metabolic parameters in chronic HCV.

Methods: Adiponectin and tumour necrosis factor-alpha (TNF-alpha) levels, HCV genotypes, HCV-RNA, IR (HOMA-IR), body mass index and liver steatosis and fibrosis were assessed in 161 non-diabetic chronic HCV patients.

Results: Chronic HCV patients with steatosis showed lower serum adiponectin levels and higher levels of TNF-alpha, HOMA, alanine aminotransferase, gamma-glutamiltransferase and Histological Activity Index (HAI) and fibrosis scores. Low adiponectin levels were independently associated with grades of steatosis and HOMA-IR. Higher tumour necrosis factor-alpha levels were observed in patients with low adiponectin levels. The extension of steatosis was inversely correlated with adiponectin levels. A correlation between grade of steatosis with HOMA-IR and fibrosis was observed. HCV genotype 3-infected patients showed lower adiponectin levels than those with other genotypes. An independent predictor of low adiponectin levels in genotype 3 infection was the extension of steatosis. Liver fibrosis score was associated with steatosis, HAI and age.

Conclusions: Chronic HCV patients with steatosis showed a serum adiponectin/TNF-alpha imbalance that is associated with IR. Reduced adiponectin levels may be involved in the pathogenesis of steatosis, which in turn accelerates progression of fibrosis in chronic HCV.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adiponectin / metabolism*
  • Adolescent
  • Adult
  • Aged
  • Blood Glucose / metabolism*
  • Fatty Liver / blood
  • Fatty Liver / etiology*
  • Female
  • Genotype
  • Hepatitis C, Chronic / blood
  • Hepatitis C, Chronic / complications*
  • Humans
  • Insulin Resistance / physiology*
  • Male
  • Middle Aged
  • Tumor Necrosis Factor-alpha / metabolism*

Substances

  • Adiponectin
  • Blood Glucose
  • Tumor Necrosis Factor-alpha