Leptin is known to regulate feeding behavior and has therefore been postulated as a mediator of anorexia associated with acute and chronic inflammation. Both leptin mRNA, and leptin protein, have also been found in the gastric epithelium.
A research team from the Fukui Medical University in Fukui, Japan, has now examined the effect of H. pylori infection on gastric leptin expression to investigate the pathophysiological role of gastric leptin.
The study examined surgically resected human stomach tissue using immunohistochemistry and reverse transcriptase-polymerase chain reaction (RT-PCR) techniques 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.
| Gastric leptin expression is raised by H. pylori infection.|
These samples were subjected to quantitative RT-PCR to examine the effect of eradication therapy on leptin expression in the gastric fundic mucosa.
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.
"Leptin is present in the human gastric mucosa", said Dr T. Azuma, one of the report authors.
"Gastric leptin may play a role in weight gain after eradication of H. pylori infection," he added, "but may have a local rather than a systemic action."