Hepatitis C May Have Causal Role in Insulin Resistance
THURSDAY, April 29 (HealthDay News) -- Suppression of hepatitis C virus (HCV) is associated with improved insulin resistance (IR), suggesting that the virus may play a causal role in IR, according to research published in the May issue of Clinical Gastroenterology and Hepatology.
Aymin Delgado-Borrego, M.D., of the University of Miami, and colleagues studied 96 subjects in the Hepatitis C Antiviral Long-Term Treatment against Cirrhosis (HALT-C) trial to determine if HCV infection plays a role in diabetes and IR. The subjects, who all had advanced hepatic fibrosis and carried non-3 HCV genotypes, underwent pegylated interferon and ribavirin therapy for 24 weeks, then were categorized by response to therapy as indicated by HCV RNA levels at week 20: 38 non-responders (<1 log10 decline), 37 partial responders (≥1 log10 decline but detectable HCV RNA), and 21 complete responders (no detectable HCV RNA). The change in IR was measured by homeostasis model assessment (HOMA2-IR).
When the researchers adjusted for baseline HOMA2-IR only, they found that the mean HOMA2-IR differences were: −2.23 for complete responders, −0.90 for partial responders, and +0.18 for non-responders. This improvement was found to be independent of age, gender, ethnicity, body mass index, fibrosis, duration of infection and medications used, and could not be accounted for by tumor necrosis factor-alpha or adiponectin.
"These findings provide additional in vivo support for a causal role of HCV in the development of IR. Further study will be necessary to clarify the mechanisms of HCV-associated IR and to evaluate the effects of early identification and management of IR in HCV infection," the authors write.
Abstract
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