title: Altered expression of glucagon-like peptide-1 and dipeptidyl peptidase IV in patients with HCV-related glucose intolerance.
abstract: OBJECTIVE
  The pathogenesis of hepatitis C virus (HCV)-associated glucose intolerance remains unclear. Glucagon-like peptide-1 (GLP-1), a gut hormone, synthesizes hepatic glycogen and is inactivated by dipeptidyl peptidase IV (DPPIV). The aims of this study were to investigate the alterations in the expression of GLP-1 and DPPIV in HCV-associated glucose intolerance.
  
  
  METHODS
  We enrolled patients with HCV- or hepatitis B virus (HBV)-related liver disease (n = 94 and 37, respectively), patients with inflammatory bowel disease (IBD; n = 14) as disease controls, and healthy controls (n = 48). The serum or tissue GLP-1 and DPPIV expression levels were determined by enzyme immunoassay, immunoblotting, or immunostaining. The hepatic glycogen content was assayed by periodic acid-Schiff staining.
  
  
  RESULTS
  The serum GLP-1 levels were significantly decreased in the HCV group (4.9 +/- 0.3 ng/mL) than those in the controls (7.5 +/- 0.6 ng/mL), the HBV group (7.0 +/- 0.5 ng/mL), or the IBD group (10.8 +/- 1.0 ng/mL, P < 0.01). Although the ileum GLP-1 expression was not significantly different between the controls and the HCV group, the DPPIV expression was significantly increased in the ileum, liver, and serum in the HCV group. Hepatic glycogen content was decreased to a greater extent in the HCV group than that in the HBV group (127.5 +/- 5.3 vs 187.7 +/- 6.6 arbitrary units; n = 19, P < 0.01).
  
  
  CONCLUSIONS
  We demonstrated the altered expressions of GLP-1 and DPPIV in patients with HCV-associated glucose intolerance. Since hepatic glycogen synthesis, a GLP-1 action, was impaired, the altered expressions of GLP-1 and DPPIV may be involved in the development of HCV-associated glucose intolerance.
authors.affiliation: Department of Medicine, Kurume University School of Medicine, Kurume, Japan.
authors.forename: Minoru
authors.initials: M
authors.lastname: Itou
authors.forename: Takumi
authors.initials: T
authors.lastname: Kawaguchi
authors.forename: Eitaro
authors.initials: E
authors.lastname: Taniguchi
authors.forename: Shuji
authors.initials: S
authors.lastname: Sumie
authors.forename: Tetsuharu
authors.initials: T
authors.lastname: Oriishi
authors.forename: Keiichi
authors.initials: K
authors.lastname: Mitsuyama
authors.forename: Osamu
authors.initials: O
authors.lastname: Tsuruta
authors.forename: Takato
authors.initials: T
authors.lastname: Ueno
authors.forename: Michio
authors.initials: M
authors.lastname: Sata
mesh_terms: D000328:Adult; D018819:Dipeptidyl Peptidase 4 / Q000097:blood / Q000378:metabolism*; D005215:Fasting / Q000097:blood; D052216:Glucagon-Like Peptide 1 / Q000097:blood / Q000378:metabolism*; D005947:Glucose / Q000378:metabolism; D018149:Glucose Intolerance; D006003:Glycogen / Q000378:metabolism; D006509:Hepatitis B / Q000097:blood / Q000378:metabolism; D006526:Hepatitis C / Q000097:blood / Q000378:metabolism / Q000503:physiopathology*; D006801:Humans; D007082:Ileum / Q000378:metabolism; D015151:Immunoblotting; D007150:Immunohistochemistry; D015212:Inflammatory Bowel Diseases / Q000097:blood / Q000378:metabolism; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D008099:Liver / Q000378:metabolism / Q000503:physiopathology; D008875:Middle Aged
chemical_list: D007328:Insulin; D052216:Glucagon-Like Peptide 1; D006003:Glycogen; D018819:Dipeptidyl Peptidase 4; D005947:Glucose