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Gastric secretion

Schubert, Mitchell L.a,b

Current Opinion in Gastroenterology: November 2014 - Volume 30 - Issue 6 - p 578–582
doi: 10.1097/MOG.0000000000000125
STOMACH AND DUODENUM: Edited by Mitchell L. Schubert

Purpose of review This review summarizes the past year's literature regarding the neural, paracrine, hormonal, and intracellular regulation of gastric acid secretion.

Recent findings Gastric acid facilitates the digestion of protein as well as the absorption of iron, calcium, vitamin B12, and certain medications. High gastric acidity, in combination with pepsin and lipase, kills ingested microorganisms and may play a role in preventing bacterial overgrowth, enteric infection, and possibly spontaneous bacterial peritonitis, community-acquired pneumonia, and infection with Mycobacterium tuberculosis. Stimulants of acid secretion include histamine, gastrin, acetylcholine, and ghrelin. Inhibitors include somatostatin, gastric inhibitory polypeptide, calcitonin gene-related peptide, and adrenomedullin. Helicobacter pylori stimulates or inhibits depending upon the time course of infection and the area of the stomach predominantly infected. Proteins implicated in H-K-ATPase membrane trafficking include myosin IIB, F-actin, ezrin, and Rab GTPases.

Summary Our understanding of the regulation of gastric acid secretion continues to advance. Such knowledge is crucial for the management of acid-peptic disorders and the development of novel medications, such as cholecystokinin-2 receptor antagonists.

aDivision of Gastroenterology, Department of Medicine, Virginia Commonwealth University Health System

bDivision of Gastroenterology, Department of Medicine, Hunter Holmes McGuire Veterans Affairs Medical Center, Richmond, Virginia, USA

Correspondence to Mitchell L. Schubert, MD, Gastroenterology Section, McGuire VAMC, Code 111N, 1201 Broad Rock Blvd., Richmond, VA 23249, USA. Tel: +1 804 675 5021; fax: +1 804 675 5816; e-mail: Mitchell.Schubert@va.gov

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