Eradication of hepatitis C virus by interferon improves whole-body insulin resistance and hyperinsulinaemia in patients with chronic hepatitis C

Liver Int. 2009 Jul;29(6):871-7. doi: 10.1111/j.1478-3231.2009.01993.x. Epub 2009 Feb 26.

Abstract

Background/aims: To investigate whether eradication of hepatitis C virus (HCV) by interferon (IFN) therapy influences systemic glucose metabolism.

Methods: Seventy-two patients with chronic hepatitis C were enrolled in this study. Patients received IFN therapy and were classified into two groups: sustained responders (n=48) and nonsustained responders (n=24). We analysed systemic glucose metabolism in terms of the following indices: homeostasis model assessment for insulin resistance (HOMA-IR) and beta-cell function (HOMA-beta), insulinogenic index (II), composite insulin sensitivity index (ISI composite) and the area under the curve of plasma glucose (PG-AUC) and serum insulin (SI-AUC) in oral glucose tolerance tests. In 28 sustained responders and 16 nonsustained responders, serum levels of soluble tumour necrosis factor receptor 2 (sTNFR2) were measured. Indices were determined before and 6 months after therapy.

Results: In the sustained responders, HOMA-beta (P=0.0004) and SI-AUC (P=0.002) were significantly decreased and the ISI composite was increased (P=0.009), although there were no significant changes in HOMA-IR, II or PG-AUC. Serum sTNFR2 levels decreased significantly after therapy in sustained responders (P=0.001). In the nonsustained responders, there were no changes in any index.

Conclusions: Eradication of HCV by IFN therapy could improve whole-body insulin resistance and insulin hypersecretion with reduced serum TNF-alpha levels.

MeSH terms

  • Adult
  • Female
  • Glucose / metabolism
  • Hepacivirus / drug effects*
  • Hepatitis C, Chronic / complications
  • Hepatitis C, Chronic / drug therapy*
  • Homeostasis / drug effects
  • Homeostasis / physiology
  • Humans
  • Hyperinsulinism / complications
  • Hyperinsulinism / drug therapy*
  • Insulin Resistance / physiology*
  • Interferons / pharmacology*
  • Interferons / therapeutic use
  • Liver / pathology
  • Male
  • Middle Aged
  • Receptors, Tumor Necrosis Factor, Type II / blood
  • Statistics, Nonparametric
  • Treatment Outcome

Substances

  • Receptors, Tumor Necrosis Factor, Type II
  • Interferons
  • Glucose