title: Effect of Helicobacter pylori infection on ghrelin expression in human gastric mucosa.
abstract: OBJECTIVE
  One of the counter-effects of Helicobacter pylori eradication therapy is subsequent obesity. Ghrelin is a recently discovered growth hormone releasing peptide. This endogenous secretagogue increases appetite and facilitates fat storage. The majority of circulating ghrelin is produced in the gastric mucosa. Therefore, we aimed at investigating changes in ghrelin immunoreactivity in gastric mucosa tissues of patients infected with H. pylori.
  
  
  METHODS
  Sixty-one patients with H. pylori infection (25 cases each of duodenal and gastric ulcer, and 11 cases of gastritis) and 22 healthy controls without H. pylori infection were included in the study. H. pylori-infected patients received standard proton pump-based triple therapy followed by histological examination and (13)C-urea breath test to confirm H. pylori eradication. H. pylori was eradicated in 50 out of 61 patients. Biopsy specimens were obtained from antrum and corpus before and 3 months following eradication. Ghrelin expression was evaluated immunohistochemically with an anti-ghrelin antibody, and the number of ghrelin-positive cells determined per 1 mm(2) of the lamina propria mucosa.
  
  
  RESULTS
  There was no relationship between ghrelin immunoreactivity and body weight or body mass index for healthy controls. The number of ghrelin-positive cells was significantly lower for H. pylori-infected patients than for healthy controls. However, the ghrelin-positive cell number increased significantly following H. pylori eradication without significant change in severity of atrophy.
  
  
  CONCLUSIONS
  These data indicated that H. pylori infection affected ghrelin expression. After H. pylori eradication, gastric tissue ghrelin concentration increased significantly. This could lead to the increased appetite and weight gain seen following H. pylori eradication.
authors.affiliation: Third Department of Internal Medicine, Division of Surgical Pathology, Nippon Medical School Hospital, Tokyo, Japan.
authors.forename: Atsushi
authors.initials: A
authors.lastname: Tatsuguchi
authors.forename: Kazumasa
authors.initials: K
authors.lastname: Miyake
authors.forename: Katya
authors.initials: K
authors.lastname: Gudis
authors.forename: Seiji
authors.initials: S
authors.lastname: Futagami
authors.forename: Taku
authors.initials: T
authors.lastname: Tsukui
authors.forename: Ken
authors.initials: K
authors.lastname: Wada
authors.forename: Teruyuki
authors.initials: T
authors.lastname: Kishida
authors.forename: Yuh
authors.initials: Y
authors.lastname: Fukuda
authors.forename: Yuichi
authors.initials: Y
authors.lastname: Sugisaki
authors.forename: Choitsu
authors.initials: C
authors.lastname: Sakamoto
mesh_terms: D000328:Adult; D000368:Aged; D004381:Duodenal Ulcer / Q000378:metabolism / Q000382:microbiology; D005260:Female; D005753:Gastric Mucosa / Q000378:metabolism* / Q000473:pathology; D005756:Gastritis / Q000378:metabolism / Q000382:microbiology; D054439:Ghrelin; D016481:Helicobacter Infections / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology; D016480:Helicobacter pylori; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D036361:Peptide Hormones / Q000378:metabolism*; D013276:Stomach Ulcer / Q000378:metabolism / Q000382:microbiology
chemical_list: D054439:Ghrelin; D036361:Peptide Hormones