Gastric leptin and Helicobacter pylori infection

Background-Leptin regulates feeding behaviour and therefore may be a mediat or of anorexia associated with acute and chronic inflammation. Recently, le ptin mRNA and leptin protein were found in the gastric epithelium. Aim-The aim of the present study was to examine the effect of Helicobacter pylori infection on gastric leptin expression to investigate the pathophysi ological role of gastric leptin. Methods-Surgically resected human stomach tissues were subjected to immunoh istochemistry and reverse transcriptase-polymerase chain reaction (RT-PCR) to check for the presence of leptin in the human gastric epithelium. A tota l of 201 H pylori positive patients with chronic gastritis underwent eradic ation therapy for H pylori and were examined for the effect of infection cu re in terms of body mass index (BMI) and serum leptin levels. Biopsy specim ens from the gastric fundic mucosa were obtained from 40 of the 201 patient s before and three months after eradication therapy. These samples were sub jected 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 gastri c fundic mucosa. H pylori infection significantly increased gastric leptin expression. In addition, cure of H pylori infection significantly reduced g astric leptin expression, with a concomitant increase in BMI. In contrast, serum leptin levels did not change significantly after cure of H pylori inf ection. Conclusion-Leptin is present in the human gastric mucosa. Gastric leptin ma y play a role in weight gain after eradication of H pylori infection. Gastr ic leptin may have a local rather than systemic action.