Insulin Resistance and Liver Injury in Patients with Hepatitis C Are Not Associa

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Insulin Resistance and Liver Injury in Patients with Hepatitis C Are

Not Associated with Virus-Specific Changes in Adipocytokines

There is a growing body of evidence linking hepatitis C virus (HCV)

infection with metabolic abnormalities including type 2 diabetes

mellitus. However, the role of adipocytokines in HCV-associated

insulin resistance it is not yet clear

Adipocytokines are chemical messengers produced by adipose (fat)

tissue. They include tumor necrosis factor alpha (TNF-alpha),

interleukin 6 (IL-6), leptin, and adiponectin.

As reported in the July 2007 issue of Hepatology, Australian

researchers tested the hypothesis that these adipocytokines

contribute to chronic HCV-associated insulin resistance and liver

injury.

The investigators first compared the serum adipocytokine levels and

homeostasis model assessment of insulin resistance (HOMA-IR) scores

of 154 untreated, non-diabetic, HCV-infected men with stage 0-2

(absent to moderate) liver fibrosis versus those of 75 healthy HCV

negative volunteers matched for age, body mass index (BMI), and waist-

to-hip ratio.

Next, they examined whether adipocytokine levels were associated with

the extent of hepatic steatosis, portal/periportal inflammation, and

fibrosis in the total cohort of 240 HCV-infected men.

Results

• Significantly higher HOMA-IR scores (2.12 vs 1.63) and levels of

TNF-alpha (1.28 vs 0.60 pg/mL) and IL-6 (2.42 vs 1.15 pg/mL) were

noted in the HCV-infected cohort compared with HCV-uninfected control

subjects.

• However, there were no significant differences in leptin and

adiponectin concentrations.

• By multiple linear regression, independent predictors of a higher

HOMA-IR score included BMI and serum leptin (positive correlation)

and serum adiponectin (negative correlation), but not TNF-alpha or IL-

6.

• Only TNF-alpha levels were correlated with the extent of

histological injury (portal/periportal inflammation).

Conclusion

" Whereas leptin and adiponectin contribute to insulin resistance,

none of the adipocytokines accounted for the elevated insulin

resistance in HCV-infected subjects, " the authors concluded. " The

adipocytokines were not associated with histological features of

chronic HCV infection except for TNF-alpha which correlated with

portal/periportal inflammation. "

Based on these results, they suggested, " HCV-associated insulin

resistance is most likely an adipocytokine-independent effect of the

virus to modulate insulin sensitivity. "