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  3. Insulin Resistance In Chronic Hepatitis C: Association With Genotypes 1 And 4, Serum Hcv Rna Level, And Liver Fibrosis.
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  3. Insulin Resistance In Chronic Hepatitis C: Association With Genotypes 1 And 4, Serum Hcv Rna Level, And Liver Fibrosis.

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Insulin resistance in chronic hepatitis C: association with genotypes 1 and 4, serum HCV RNA level, and liver

Rami Moucari1, Tarik Asselah, Dominique Cazals-Hatem

  • 1AP-HP, Hôpital Beaujon, Service d'Hépatologie, Clichy F-92110, France.

Gastroenterology
|January 1, 2008

View abstract on PubMed

Summary
This summary is machine-generated.

Insulin resistance (IR) is common in chronic hepatitis C (CHC) patients, particularly with genotypes 1 and 4. IR is linked to significant liver fibrosis, independent of steatosis.

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Area of Science:

  • Hepatology
  • Metabolic Disorders
  • Virology

Background:

  • Chronic hepatitis C (CHC) is a significant global health concern.
  • Insulin resistance (IR) is increasingly recognized as a factor in liver disease progression.
  • The relationship between IR, hepatitis C virus (HCV) characteristics, and liver disease severity requires further investigation.

Purpose of the Study:

  • To investigate the association between insulin resistance (IR) and hepatitis C virus (HCV) genotypes, viral load, and liver fibrosis stage.
  • To compare the prevalence of IR in CHC patients versus chronic hepatitis B (CHB) patients.
  • To identify independent predictors of IR and significant liver fibrosis in CHC.

Main Methods:

  • Prospective cohort study of 600 patients (500 CHC, 100 CHB) undergoing liver biopsy.
  • Assessment of IR using the Homeostasis Model for Assessment of Insulin Resistance (HOMA-IR) and metabolic syndrome components.
  • Logistic regression analysis to determine factors associated with IR and significant fibrosis in non-diabetic, non-cirrhotic CHC patients.

Main Results:

  • IR was present in 32.4% of non-diabetic CHC patients and associated with metabolic syndrome, HCV genotypes 1 and 4, significant fibrosis, and severe steatosis.
  • In CHC patients without metabolic syndrome or significant fibrosis, IR (15%) was linked to genotypes 1 and 4, high HCV RNA levels, and necroinflammation.
  • Significant fibrosis was observed in 51.1% of non-cirrhotic CHC patients, associated with male sex, age >40, IR, necroinflammation, and severe steatosis.
  • IR was significantly less frequent in CHB patients compared to matched CHC patients (5% vs. 35%, P < .001).

Conclusions:

  • Insulin resistance is a distinct feature of CHC, strongly associated with HCV genotypes 1 and 4 and elevated HCV RNA levels.
  • Significant liver fibrosis in CHC is independently associated with IR, even when steatosis is absent.
  • IR is less prevalent in CHB compared to CHC, suggesting a specific role in HCV pathogenesis.