Gastric secretionHou, Wei; Schubert, Mitchell LCurrent Opinion in Gastroenterology: November 2006 - Volume 22 - Issue 6 - p 593–598 doi: 10.1097/01.mog.0000245538.43142.87 Stomach and duodenum Abstract Author Information Purpose of review: To summarize the literature over the past year on the regulation of gastric exocrine and endocrine secretion. Recent findings: Gastric acid secretion by parietal cells is precisely regulated by overlapping neural, hormonal, and paracrine pathways, both centrally and peripherally. Too much acid can induce gastroduodenal injury. Too little acid can interfere with the absorption of iron, calcium, vitamin B12, and certain drugs as well as predispose the patient to enteric infection. A number of peptides implicated in the central control of food intake such as ghrelin, orexin, and leptin are present in the stomach and are capable of modulating acid secretion. The precise mechanisms whereby Helicobacter pylori produces perturbations in acid secretion are not precisely known but appear to involve changes in somatostatin and perhaps ghrelin secretion. Both gastrin and gastrin-receptor knockout mice as well as gastrin-overexpressing and cAMP-overexpressing mice develop gastric atrophy; gastric atrophy is associated with antiparietal cell antibodies and may be a model for autoimmune gastritis. Summary: A better understanding of the pathways and mechanisms regulating acid secretion as well as the development of genetically engineered mouse models should lead to new strategies to prevent and treat a variety of gastric disorders, including peptic ulcer disease, neoplasia, and autoimmune gastritis. Department of Medicine, Division of Gastroenterology, Virginia Commonwealth University's Medical College of Virginia and McGuire Veterans Affairs Medical Center, Richmond, Virginia, USA Correspondence to Mitchell L. Schubert, MD, McGuire VAMC, code 111N, Gastroenterology Division, 1201 Broad Rock Blvd, Richmond, VA 23249, USA Tel: +1 804 675 5021; fax: +1 804 675 5816; e-mail: email@example.com © 2006 Lippincott Williams & Wilkins, Inc.