title: Insulin resistance and hepatitis C virus: a case-control study of non-obese, non-alcoholic and non-steatotic hepatitis virus carriers with persistently normal serum aminotransferase.
abstract: OBJECTIVE
  Recent studies using transgenic mouse models have demonstrated that the presence of hepatitis C virus (HCV) singularly induces insulin resistance (IR). When evaluated in humans, the exclusion of other factors influencing IR, such as obesity, alcohol intake, hepatic inflammation and steatosis is needed, but only few studies have been performed to these ends. Therefore, we aimed at exploring the singular effects of HCV on glucose metabolism through analysis of HCV carriers with persistently normal serum aminotransferase.
  
  
  METHODS
  Non-obese, non-diabetic and non-alcoholic HCV carriers (n=30) were enrolled with 30 hepatitis B virus carriers matched by age, gender, body mass index and waist-to-hip ratio. All patients maintained normal serum aminotransferase (<30 U/L), hyaluronic acid (<50 ng/ml) and platelet count (>150 x 10(3)/microl) for more than 5 years without additional treatments, and had no signs of steatosis. We then compared fasting plasma glucose, serum insulin and adiponectin, and homoeostasis model assessment of IR (HOMA-IR) and HOMA-beta indices between the groups.
  
  
  RESULTS
  There were no significant differences in IR/secretion-associated markers or serum adiponectin. Multivariate analysis demonstrated that the presence of HCV was not an independent predictor of IR. HOMA-IR was strongly correlated with waist circumferences and serum gamma-glutamyltransferase in HCV carriers, but not with serum aminotransferase, high-sensitivity C-reactive protein, hyaluronic acid or HCV core antigen.
  
  
  CONCLUSIONS
  These results suggest that the presence of HCV alone does not affect IR. Coexistence of hepatitis, steatosis and/or fibrosis may be important to the pathogenesis of IR induced by chronic HCV infection.
authors.affiliation: Department of Metabolic Regulation, Shinshu University Graduate School of Medicine, Matsumoto, Japan. naopi@hsp.md.shinshu-u.ac.jp
authors.forename: Naoki
authors.initials: N
authors.lastname: Tanaka
authors.forename: Tadanobu
authors.initials: T
authors.lastname: Nagaya
authors.forename: Michiharu
authors.initials: M
authors.lastname: Komatsu
authors.forename: Akira
authors.initials: A
authors.lastname: Horiuchi
authors.forename: Goro
authors.initials: G
authors.lastname: Tsuruta
authors.forename: Haruaki
authors.initials: H
authors.lastname: Shirakawa
authors.forename: Takeji
authors.initials: T
authors.lastname: Umemura
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Ichijo
authors.forename: Akihiro
authors.initials: A
authors.lastname: Matsumoto
authors.forename: Kaname
authors.initials: K
authors.lastname: Yoshizawa
authors.forename: Toshifumi
authors.initials: T
authors.lastname: Aoyama
authors.forename: Kendo
authors.initials: K
authors.lastname: Kiyosawa
authors.forename: Eiji
authors.initials: E
authors.lastname: Tanaka
mesh_terms: D000328:Adult; D000368:Aged; D000410:Alanine Transaminase / Q000097:blood*; D002353:Carrier State; D016022:Case-Control Studies; D005260:Female; D019694:Hepatitis B, Chronic / Q000097:blood / Q000503:physiopathology; D019698:Hepatitis C, Chronic / Q000097:blood* / Q000503:physiopathology; D006801:Humans; D007328:Insulin / Q000378:metabolism; D007333:Insulin Resistance; D000078790:Insulin Secretion; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis
chemical_list: D007328:Insulin; D000410:Alanine Transaminase