Chronic Hepatitis C Is Associated With Peripheral Rather Than Hepatic Insulin Resistance

Associations of chronic hepatitis C with metabolic and cardiac outcomes

“…9 In addition, recent evidence suggests involvement of the striated muscle in the pathogenesis of IR in patients with CH-C. 10 The consequences of IR and DM in HCV-infected patients can be divided into those that affect liver disease outcomes and those affecting nonliver related outcomes. 11 HCV patients with DM or IR tend to have more advanced hepatic fibrosis, hepatocellular carcinoma and lower efficacy of treatment regimens. 12 In addition to metabolic conditions (DM and IR), HCV has also been associated with arthrosclerosis and coronary artery disease.…”

Successful Hepatitis C Antiviral Therapy Induces Remission of Type 2 Diabetes: A Case Report

“…HCV directly impacts insulin signaling by interacting with specific proteins such as serine/threonine kinases that subsequently lead to inhibition or increased degradation of insulin signaling molecules [6,23]. HCV may also indirectly cause insulin resistance in the periphery by inducing the production of pro-inflammatory cytokines that impair insulin signaling pathways in uninfected tissues [20]. Changes in metabolic parameters described with chronic HCV infection differ by genotype, suggesting that the mechanisms by which these signaling molecules are impacted are genotype-dependent.…”

“…HCV infection is specific to the liver. However, insulin sensitivity appears to be impaired both in the liver and the periphery [20,21]. HCV impairs insulin signaling through direct and indirect mechanisms [22].…”

Homeostasis model assessment of insulin resistance does not seem to predict response to telaprevir in chronic hepatitis C in the REALIZE trial

“…Plasma HCV RNA was measured using the COBAS TaqMan assay, v. 2.0 (Roche, Switzerland; lower limit of quantification 25 IU/mL and lower limit of detection 10 IU/mL) at screening, baseline, day 3, during weeks 1, 2, 4, 5,6,8,10,12,14,16,20,24,36, and 48, at early discontinuation, at follow-up visits 4, 12, and 24 weeks after end of treatment and at week 72, even in patients who discontinued early. SVR was defined as having undetectable (<25 IU/mL undetectable) HCV RNA at 24 weeks after the last planned dose of study medication.…”

“…2,3 Proposed mechanisms for HCV-related IR and diabetes mellitus include direct hepatic effects [4][5][6] and potential contributions from extrahepatic organs. 7,8 In HCV-infected patients, IR appears to influence disease progression and response to treatment with peginterferon alpha and ribavirin. 9,10 IR appears to be associated with a lower rate of sustained virologic response (SVR) in patients receiving peginterferon alpha and ribavirin.…”