title: Gastric leptin and Helicobacter pylori infection.
abstract: BACKGROUND
  Leptin regulates feeding behaviour and therefore may be a mediator of anorexia associated with acute and chronic inflammation. Recently, leptin mRNA and leptin protein were found in the gastric epithelium.
  
  
  OBJECTIVE
  The aim of the present study was to examine the effect of Helicobacter pylori infection on gastric leptin expression to investigate the pathophysiological role of gastric leptin.
  
  
  METHODS
  Surgically resected human stomach tissues were subjected to immunohistochemistry and reverse transcriptase-polymerase chain reaction (RT-PCR) to check for the presence of leptin in the human gastric epithelium. A total of 201 H pylori positive patients with chronic gastritis underwent eradication therapy for H pylori and were examined for the effect of infection cure in terms of body mass index (BMI) and serum leptin levels. Biopsy specimens from the gastric fundic mucosa were obtained from 40 of the 201 patients before and three months after eradication therapy. These samples were subjected to quantitative RT-PCR to examine the effect of eradication therapy on leptin expression in the gastric fundic mucosa.
  
  
  RESULTS
  Leptin immunoreactive cells were detected in the lower half of the gastric fundic glands and a leptin PCR product was also found in the gastric fundic mucosa. H pylori infection significantly increased gastric leptin expression. In addition, cure of H pylori infection significantly reduced gastric leptin expression, with a concomitant increase in BMI. In contrast, serum leptin levels did not change significantly after cure of H pylori infection.
  
  
  CONCLUSIONS
  Leptin is present in the human gastric mucosa. Gastric leptin may play a role in weight gain after eradication of H pylori infection. Gastric leptin may have a local rather than systemic action.
authors.affiliation: Second Department of Internal Medicine, Fukui Medical University, Fukui, Japan. azuma@fmsrsa.fukui-med.ac.jp
authors.forename: T
authors.initials: T
authors.lastname: Azuma
authors.forename: H
authors.initials: H
authors.lastname: Suto
authors.forename: Y
authors.initials: Y
authors.lastname: Ito
authors.forename: M
authors.initials: M
authors.lastname: Ohtani
authors.forename: M
authors.initials: M
authors.lastname: Dojo
authors.forename: M
authors.initials: M
authors.lastname: Kuriyama
authors.forename: T
authors.initials: T
authors.lastname: Kato
mesh_terms: D000328:Adult; D000658:Amoxicillin / Q000627:therapeutic use; D000897:Anti-Ulcer Agents / Q000627:therapeutic use; D015415:Biomarkers; D001706:Biopsy; D015992:Body Mass Index; D016022:Case-Control Studies; D017291:Clarithromycin / Q000627:therapeutic use; D004359:Drug Therapy, Combination / Q000627:therapeutic use; D005260:Female; D005753:Gastric Mucosa / Q000378:metabolism; D016481:Helicobacter Infections / Q000188:drug therapy / Q000378:metabolism*; D016480:Helicobacter pylori; D006801:Humans; D020738:Leptin / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D009853:Omeprazole / Q000627:therapeutic use; D020133:Reverse Transcriptase Polymerase Chain Reaction; D018709:Statistics, Nonparametric; D013274:Stomach Neoplasms / Q000378:metabolism
chemical_list: D000897:Anti-Ulcer Agents; D015415:Biomarkers; D020738:Leptin; D000658:Amoxicillin; D017291:Clarithromycin; D009853:Omeprazole