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Change of Acid Secretions, Ghrelin and Leptin, by H. pylori

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Helicobacter pylori

Abstract

When Helicobacter pylori (H. pylori) begins to colonize on the surface of gastric epithelium, H. pylori induces strong inflammatory responses and causes a transitory hypochlorhydria. The main underlying mechanisms are, first, H. pylori represses the activity of promoter of the alpha-subunit (HKα) of H+, K+-ATPase, and second, cytokines such as interleukin (IL)-1β and tumor necrosis factor (TNF)-α suppress gastric acid. Third, H. pylori-induced gastritis evokes decrease of parietal cell numbers. In the chronic H. pylori gastritis, the change of gastric acid is mainly determined by the pattern of corpus gastritis. That is, in the antral-predominant gastritis, acid secretion increases due to increase of gastrin secretion. In the situation of corpus-predominant gastritis, acid secretion is decreased similar to the acute gastritis. The acute response after H. pylori eradication includes the increase of gastric acid mainly due to the clearance of H. pylori itself and its secreted proteins, reversed activity of H+, K+-ATPase, and decrease of IL-1β and TNF-α. After this acute response phenomenon, the change of acid secretion depends on gastritis pattern. That is, in the situation of corpus-predominant gastritis, acid secretion increases slowly until 2 years depending on the severity of atrophic gastritis. In the antral-predominant gastritis, the increase of gastric acid secretion stops and it returns to normal as gastrin secretion decreases. In contrast to acid secretion, the effect of H. pylori and its eradication on ghrelin and leptin levels is under investigation.

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  1. Department of Internal Medicine, Seoul National University College of Medicine, Seoul National University Bundang Hospital, 82 Gumi-ro 173 beon-gil, Bundang-gu, Seongnam, Gyeonggi-do, 13620, South Korea

    Nayoung Kim MD, PhD & Yoon Jin Choi

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    Nayoung Kim

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Kim, N., Choi, Y.J. (2016). Change of Acid Secretions, Ghrelin and Leptin, by H. pylori . In: Kim, N. (eds) Helicobacter pylori. Springer, Singapore. https://doi.org/10.1007/978-981-287-706-2_4

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