title: Hepatitis C virus infection enhances insulin resistance induced by visceral fat accumulation.
abstract: OBJECTIVE
  To clarify the impact of visceral obesity on hepatitis C virus (HCV)-infected patients, we examined the relationship between insulin resistance development and visceral fat accumulation.
  
  
  METHODS
  We analyzed 87 HCV-infected patients with mild fibrosis (stage 1 or 2) in comparison with 125 sex- and age-matched patients with non-alcoholic fatty liver disease (NAFLD). The degree of visceral fat area (VFA; cm(2)) at the umbilical level was measured by abdominal computed tomography and divided into two grades: no visceral obesity, VFA<100 and visceral obesity, VFA>/=100. Insulin resistance was evaluated by homeostasis model assessment of insulin resistance (HOMA-IR) and the quantitative insulin sensitivity check index (QUICKI). Pancreatic beta-cell function was evaluated by homeostasis model assessment of beta-cell function (HOMA-beta). Serum soluble tumour necrosis factor (TNF)-receptors 1 and 2 and adiponectin were measured.
  
  
  RESULTS
  Insulin resistance evaluated by HOMA-IR and QUICKI was correlated with visceral fat accumulation, and was higher in HCV patients than in NAFLD patients with visceral obesity. HOMA-beta was higher in HCV patients than in NAFLD patients for each VFA grade. Serum-soluble TNF-receptors 1 and 2 were higher in HCV patients than in NAFLD patients with visceral obesity.
  
  
  CONCLUSIONS
  Hepatitis C virus infection is a risk factor for development of insulin resistance, particularly in patients with visceral obesity.
authors: Department of Internal Medicine, Saga Medical School, Saga, Japan. eguchiyu@cc.saga-u.ac.jp
authors: Yuichiro
authors: Y
authors: Eguchi
authors: Toshihiko
authors: T
authors: Mizuta
authors: Eriko
authors: E
authors: Ishibashi
authors: Yoichiro
authors: Y
authors: Kitajima
authors: Noriko
authors: N
authors: Oza
authors: Shunya
authors: S
authors: Nakashita
authors: Megumi
authors: M
authors: Hara
authors: Shinji
authors: S
authors: Iwane
authors: Hirokazu
authors: H
authors: Takahashi
authors: Takumi
authors: T
authors: Akiyama
authors: Keisuke
authors: K
authors: Ario
authors: Yasunori
authors: Y
authors: Kawaguchi
authors: Tsutomu
authors: T
authors: Yasutake
authors: Ryuichi
authors: R
authors: Iwakiri
authors: Iwata
authors: I
authors: Ozaki
authors: Akitaka
authors: A
authors: Hisatomi
authors: Takahisa
authors: T
authors: Eguchi
authors: Naofumi
authors: N
authors: Ono
authors: Kazuma
authors: K
authors: Fujimoto
mesh_terms: D052242:Adiponectin / Q000097:blood; D001774:Blood Chemical Analysis; D005234:Fatty Liver / Q000503:physiopathology*; D005260:Female; D006526:Hepatitis C / Q000503:physiopathology*; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology*; D050152:Intra-Abdominal Fat / Q000503:physiopathology*; D007564:Japan; D008099:Liver / Q000473:pathology; D008297:Male; D008954:Models, Biological; D009765:Obesity / Q000503:physiopathology*; D018124:Receptors, Tumor Necrosis Factor / Q000097:blood; D018709:Statistics, Nonparametric
chemical_list: D052242:Adiponectin; D018124:Receptors, Tumor Necrosis Factor