Effect of Helicobacter pylori infection on gastric ghrelin expression and body weight

Ghrelin is a peptide mainly produced by gastric tissue playing an important role in energy homeostasis. It has been suggested that inflammatory and atrophic events induced by Helicobacter pylori (H. pylori) infection in gastric mucosa compromise the survival of the ghrelin-producing cells. The aim of this study was to investigate the effect of H. pylori infection on gastric ghrelin expression and body weight.

Consecutive patients referred for upper endoscopy were invited to participate. Patients with H. pylori infection (determined by histology) were defined as cases and patients without infection as controls. The density of colonization was classified in mild, moderate, or severe infection. Body mass index (BMI) was calculated. Ghrelin-immunoreactive cells were quantified in gastric biopsies by immunohistochemical staining.

We studied 189 cases (92 males, 97 females) and 94 controls (55 males, 39 females). Cases were older (48.16 +/- 16.44 vs. 42.88 +/- 17.04 years, p < 0.05) and exhibited a lower percentage of ghrelin-immunoreactive cells (2.13% vs. 10.43%, p < 0.05) than controls. The prevalence of obesity was significantly lower than normal-weight among all cases, independently of the severity of infection (mild infection, 17.6% vs. 47.3%, p = 0.001; moderate-severe infection, 10.4% vs. 50%, p = 0.001). Univariate analysis showed a non-significant trend suggesting a protective effect of H. pylori against obesity. Nevertheless, BMI did not differ significantly between cases and controls.

Chronic H. pylori infection contributes to a lower percentage of gastric ghrelin-immunoreactive cells but has no effect on the body weight of infected patients.