Helicobacter pylori and gut hormones

Abstract

Helicobacter pylori infection has been found to decrease the expression of antral somatostatin and to increase the release of the acid-stimulating hormone gastrin. The reversal of these changes in gut hormones by the eradication of H. pylori, and in-vivo and in-vitro studies in animals either infected with H. pylori or exposed to H. pylori-related materials may support the somatostatin-gastrin link theory in the pathophysiology of H. pylori infection. The following mechanisms have been proposed to explain the H. pylori infection-associated changes in gut hormones; (1) ammonia produced by H. pylori and monochloramine, (2) effect on somatostatin receptor subtype-2, (3) action of lipopolysaccharide from H. pylori on somatostatin receptor, (4) inflammatory cells and mediators, and (5) bacterial strain diversity. H. pylori infection can alter gastric acid secretion in both directions. The elevated acid secretion in patients with duodenal ulcer is decreased by H. pylori eradication, and is accompanied by the normalization of gut hormones in patients whose H. pylori-induced gastritis is limited to the antrum with hyperacidity. Corpus gastritis and the subsequent development of mucosal atrophy induced by H. pylori result in decreased acid secretion, although the mechanism underlying H. pylori-induced atrophy in some subjects remains unclear. Hypoacidity enhances corpus atrophy and increases gastrin secretion, mediated via a physiological suppression of somatostatin release, features that are also observed in H. pylori infection. Therefore, the capacity of acid secretion and distribution of gastritis or atrophy should be taken into consideration when we discuss the affect of H. pylori on gut hormones.

The association between Helicobacter pylori seropositivity and risk of new-onset diabetes: a prospective cohort study

“…Several studies have reported that H. pylori seropositivity was associated with different hormones [2,[8][9][10], most of which were involved in glucose metabolism directly or indirectly [11][12][13][14][15][16][17]. To our knowledge, at least three hormones supported our results, including gastrin, leptin and ghrelin.…”

Helicobacter pylori has no effect on plasma ghrelin levels

“…H. pylori infection increases plasma gastrin concentrations during fasting, after meals, and after the infusion of bombesin or gastrin-releasing peptide (17 -19). SST deficiency had been proposed in duodenal ulcer patients before the discovery of H. pylori (3). Recent studies have clearly demonstrated that antral SST levels were decreased in H. pylori infection (20,21).…”

“…SST has an inhibitory effect on growth hormone (GH) release, and the presence of SST-containing D cells in the canine antral mucosa has been shown by Fujita and Kobayashi (4 (6). H. pylori infection has been shown to increase plasma gastrin concentrations during fasting and after meals (3).…”

“…Gastric acid secretion is also regulated by many factors involving the autonomic nervous system and gut hormones. Among several hormones affecting gastric acid secretion directly or indirectly, the most important regulatory peptides in the gastric mucosa include gastrin and somatostatin (SST) (3). SST has an inhibitory effect on growth hormone (GH) release, and the presence of SST-containing D cells in the canine antral mucosa has been shown by Fujita and Kobayashi (4 (6).…”

Ultrasonographical Evaluation of Gallbladder Functions in Helicobacter Pylori-Positive and Negative Patients

“…Following the H. pylori eradication, SST concentration becomes normal, and similarly gastrin goes back to its normal levels (4)(5)(6)(7)(8). SST inhibits the secretion of cholecystokinin, gastrin, secretine and glukagon.…”