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Gut 54:1003-1008 doi:10.1136/gut.2004.050302
  • Hepatitis

Insulin resistance is a cause of steatosis and fibrosis progression in chronic hepatitis C

  1. L Fartoux1,
  2. A Poujol-Robert2,
  3. J Guéchot3,
  4. D Wendum4,
  5. R Poupon1,
  6. L Serfaty1
  1. 1Service d’Hépatologie, Hôpital Saint-Antoine, Paris, France, and Inserm U680, Universite Pierre et Marie Curie, Paris, France
  2. 2Service d’Hépatologie, Hôpital Saint-Antoine, Paris, France
  3. 3Service de Biochimie, Hôpital Saint-Antoine, Paris, France
  4. 4Service d’Anatomo-pathologie, Hôpital Saint-Antoine, Paris, France
  1. Correspondence to:
    Dr L Serfaty
    Service d’Hépatologie, Hopital Saint-Antoine, 184 rue du Faubourg Saint-Antoine, 75571 Paris cedex 12, France; lawrence.serfatysat.ap-hop-paris.fr
  • Accepted 26 October 2004
  • Revised 1 October 2004

Abstract

Background: Insulin resistance is a frequent feature of chronic hepatitis C. Whether insulin resistance could be the cause or consequence of steatosis and fibrosis is unknown. The ability of HCV genotype 3 to promote steatosis by itself provides an unique opportunity to answer this question.

Aims: The aim of the present study was to assess the relationships between insulin resistance, steatosis, and fibrosis according to genotype in 141 non-diabetic patients with biopsy proven non-cirrhotic chronic hepatitis C.

Methods: All patients had fasting serum glycaemia and insulinaemia measurements. Insulin resistance was evaluated using the homeostasis model assessment (HOMA IR) method. Liver steatosis was determined according to hepatitis C virus genotype (1 or 3). Logistic regression and multivariate regression analysis were used to identify variables independently associated with insulin resistance, fatty liver, and fibrosis.

Results: Although steatosis and fibrosis were more severe in genotype 3 patients, median HOMA IR was significantly higher in patients with genotype 1 related steatosis than in those with genotype 3 related steatosis (2.1 v 1; p = 0.001). Independent risk factors for steatosis were insulin resistance in genotype 1 patients (p = 0.001) and viral load in genotype 3 patients (p = 0.003). Among genotype 1 patients, independent parameters associated with insulin resistance were age (p = 0.04) and steatosis (p = 0.004). Steatosis was associated with more severe fibrosis whatever the genotype (p = 0.002). Among genotype 1 patients, although there was a significant relationship between circulating insulin level and fibrosis stage (p = 0.006), only steatosis and inflammatory score were independently associated with fibrosis.

Conclusion: This study shows that insulin resistance is the cause rather than the consequence of steatosis and fibrosis in genotype 1 patients and that increased circulating insulin is a risk factor for fibrosis through insulin resistance induced steatosis.

Footnotes

  • Conflict of interest: None declared.

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