title: Eradication of hepatitis C virus by interferon improves whole-body insulin resistance and hyperinsulinaemia in patients with chronic hepatitis C.
abstract: OBJECTIVE
  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.
authors.affiliation: Department of Internal Medicine, Saga Medical School, Saga, Japan. kawaguy@cc.saga-u.ac.jp
authors.forename: Yasunori
authors.initials: Y
authors.lastname: Kawaguchi
authors.forename: Toshihiko
authors.initials: T
authors.lastname: Mizuta
authors.forename: Noriko
authors.initials: N
authors.lastname: Oza
authors.forename: Hirokazu
authors.initials: H
authors.lastname: Takahashi
authors.forename: Keisuke
authors.initials: K
authors.lastname: Ario
authors.forename: Toru
authors.initials: T
authors.lastname: Yoshimura
authors.forename: Yuichiro
authors.initials: Y
authors.lastname: Eguchi
authors.forename: Iwata
authors.initials: I
authors.lastname: Ozaki
authors.forename: Akitaka
authors.initials: A
authors.lastname: Hisatomi
authors.forename: Kazuma
authors.initials: K
authors.lastname: Fujimoto
mesh_terms: D000328:Adult; D005260:Female; D005947:Glucose / Q000378:metabolism; D016174:Hepacivirus / Q000187:drug effects*; D019698:Hepatitis C, Chronic / Q000150:complications / Q000188:drug therapy*; D006706:Homeostasis / Q000187:drug effects / Q000502:physiology; D006801:Humans; D006946:Hyperinsulinism / Q000150:complications / Q000188:drug therapy*; D007333:Insulin Resistance / Q000502:physiology*; D007372:Interferons / Q000494:pharmacology* / Q000627:therapeutic use; D008099:Liver / Q000473:pathology; D008297:Male; D008875:Middle Aged; D047889:Receptors, Tumor Necrosis Factor, Type II / Q000097:blood; D018709:Statistics, Nonparametric; D016896:Treatment Outcome
chemical_list: D047889:Receptors, Tumor Necrosis Factor, Type II; D007372:Interferons; D005947:Glucose