Chronic hepatitis C virus infection is associated with an increased prevalence of type 2 diabetes.
In this study, researchers from Australia assessed whether virus-induced insulin resistance was a mechanism for fibrogenesis in chronic hepatitis C virus infection.
The team evaluated 250 hepatitis C virus-infected subjects.
They examined the relationship between histological findings, and anthropometric and biochemical data, including insulin resistance. Insulin resistance was determined by the homeostasis model assessment (HOMA-IR).
The team also compared fasting serum insulin, C peptide, and HOMA-IR levels in 121 hepatitis C virus patients with stage 0 or 1 hepatic fibrosis and 137 healthy volunteers.
|Insulin resistance was an independent predictor of the degree of fibrosis.|
The researchers found that hepatitis C virus-infected subjects with stage 0 or 1 hepatic fibrosis had higher levels of insulin, C peptide, and HOMA-IR than the controls.
In the 250 hepatitis C virus patients, viral genotype and portal inflammation were univariate predictors of HOMA-IR.
Using multiple linear regression analysis, the team identified BMI, previous failed antiviral treatment, portal inflammatory grade, and genotype 3 status as independent predictors of HOMA-IR
Patients with genotype 3 had significantly lower HOMA-IR than other genotypes.
The team also found that HOMA-IR was an independent predictor for the degree of fibrosis, as well as the rate of fibrosis progression.
Dr Jason Hui's team concluded, "Hepatitis C virus may induce insulin resistance irrespective of the severity of liver disease, and this effect seems to be genotype specific".
"Further, our findings support the hypothesis that insulin resistance may contribute to fibrotic progression in chronic hepatitis C virus infection".