title: Helicobacter pylori infection accelerates gene expression of glicentin in the gastric mucosa. Its association with intestinal metaplasia of the stomach.
abstract: BACKGROUND
  Glicentin is an intestinal polypeptide hormone which seems to promote intestinal metaplasia (IM) in the gastric mucosa. The aim of this study was to clarify whether Helicobacter pylori infection accelerates glicentin gene expression.
  
  
  METHODS
  Glicentin mRNA was investigated by reverse-transcription polymerase chain reaction using gastric biopsies from 47 patients examined endoscopically and denying IM.
  
  
  RESULTS
  IM was observed in 18 (38.3%) cases histologically, but not in the other 29 (62.7%). Glicentin mRNA was significantly correlated with histological IM (P < 0.01) and was positively correlated with H. pylori infection (P < 0.05).
  
  
  CONCLUSIONS
  Our results indicate that H. pylori infection is associated with the induction of glicentin in the gastric mucosa, thus supporting the hypothesis that H. pylori infection accelerates IM of the stomach.
authors.affiliation: Second Dept. of Internal Medicine, Shimane Medical University, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Ishihara
authors.forename: R
authors.initials: R
authors.lastname: Fukuda
authors.forename: N
authors.initials: N
authors.lastname: Moriyama
authors.forename: N
authors.initials: N
authors.lastname: Ishimura
authors.forename: T
authors.initials: T
authors.lastname: Kaji
authors.forename: Y
authors.initials: Y
authors.lastname: Kushiyama
authors.forename: K
authors.initials: K
authors.lastname: Amano
authors.forename: K
authors.initials: K
authors.lastname: Hirakawa
authors.forename: Y
authors.initials: Y
authors.lastname: Amano
authors.forename: K
authors.initials: K
authors.lastname: Adachi
authors.forename: N
authors.initials: N
authors.lastname: Ashizawa
authors.forename: S
authors.initials: S
authors.lastname: Fukumoto
mesh_terms: D000328:Adult; D000368:Aged; D017931:DNA Primers / Q000737:chemistry; D004386:Duodenum / Q000378:metabolism / Q000382:microbiology / Q000473:pathology; D016145:Endoscopy, Digestive System; D004947:Esophagus / Q000378:metabolism / Q000382:microbiology / Q000473:pathology; D005260:Female; D005753:Gastric Mucosa / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D015870:Gene Expression; D053771:Glicentin; D005934:Glucagon / Q000096:biosynthesis*; D004763:Glucagon-Like Peptides; D016481:Helicobacter Infections / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D016480:Helicobacter pylori / Q000302:isolation & purification*; D006801:Humans; D008297:Male; D008679:Metaplasia / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D008875:Middle Aged; D010446:Peptide Fragments / Q000096:biosynthesis*; D016133:Polymerase Chain Reaction; D011498:Protein Precursors / Q000096:biosynthesis*; D012333:RNA, Messenger / Q000032:analysis; D012189:Retrospective Studies
chemical_list: D017931:DNA Primers; D010446:Peptide Fragments; D011498:Protein Precursors; D012333:RNA, Messenger; D004763:Glucagon-Like Peptides; D053771:Glicentin; D005934:Glucagon