Gastric secretion

Purpose of review This review summarizes the past year's literature regarding the regulation and assessment of gastric acid secretion. Recent findings Gastric acid secretion is regulated by biologic agents produced and released by enteroendocrine cells and neurons as well as by exogenously administered substances and infection. Too much acid can lead to gastroesophageal reflux disease, peptic ulcer disease, and stress-related erosion/ulcer disease. Too little acid can interfere with the absorption of certain nutrients, predispose to enteric infection, and interfere with the absorption of some medications. Gastrin, histamine, gastrin-releasing peptide, ghrelin, orexin, and glucocorticoids stimulate whereas leptin, glucagon-like peptide 1, and Helicobacter pylori inhibit acid secretion. Helicobacterpylori inhibits the transcriptional activity of H (+) K (+) -ATPase, the proton pump of the parietal cell. Summary A better understanding of the pathways and mechanisms regulating gastric acid secretion should lead to improved management of patients with acid-induced disorders as well as those who secrete too little acid.