Gastric secretion

This review summarizes the past year's literature regarding the regulation of gastric exocrine and endocrine secretion, both basic science and clinical.

Gastric acid secretion facilitates the digestion of protein as well as the absorption of iron, calcium, vitamin B12, and certain medications as well as prevents bacterial overgrowth, enteric infection, and possibly community-acquired pneumonia, spontaneous bacterial peritonitis, and IgE-mediated food allergy. It is regulated by neural (e.g., pituitary adenylate cyclase-activating peptide), hormonal (e.g., gastrin, ghrelin, and apelin), and paracrine (e.g., histamine) pathways as well as by chemical (e.g., amino acids) and bacterial stimuli (e.g., Helicobacter pylori). Novel peptides, which may possess physiologic function, have been identified in gastric mucosal neuroendocrine cells including parathyroid hormone-like hormone in histamine-secreting enterochromaffin-like cells and hepcidin in acid-secreting parietal cells. The secretion of hydrochloric acid by parietal cells involves translocation of the proton pump, HK-ATPase, to the apical membrane along with activation of apical chloride and potassium channels. Serum markers include chromogranin A for neuroendocrine tumors, pepsinogen I for gastric atrophy, and pepsinogen II for H. pylori infection.

We continue to make progress in our understanding of the regulation of gastric acid secretion in health and disease.