Document Detail


Gastric secretion.
MedLine Citation:
PMID:  20838342     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
PURPOSE OF REVIEW: This review summarizes the past year's literature regarding the regulation of gastric exocrine and endocrine secretion at the central, peripheral, and cellular levels.
RECENT FINDINGS: Gastric acid secretion is an intricate and dynamic process that is regulated by neural (efferent and afferent), hormonal (e.g., gastrin), and paracrine (e.g., histamine, ghrelin, somatostatin) pathways as well as mechanical (e.g., distension) and chemical (e.g., protein, glutamate, coffee, and ethanol) stimuli. Secretion of hydrochloric acid by the parietal cell involves recruitment and fusion of HK-adenosine triphosphatase (HK-ATPase)-containing cytoplasmic tubulovesicles with the apical membrane with subsequent electroneutral transport of hydronium ions in exchange for potassium; the source of the latter is the potassium channel, KCNQ1. Concomitantly, chloride exits via the cystic fibrosis transmembrane regulator. Inhibition of the HK-ATPase by proton pump inhibitors leads to a compensatory hypergastrinemia which, if prolonged, results in parietal and enterochromaffin-like cell hyperplasia. The clinical consequence is rebound acid secretion which may induce dyspeptic symptoms in healthy individuals and exacerbate reflux symptoms in patients with gastroesophageal reflux disease.
SUMMARY: We continue to make progress in our understanding of the regulation of gastric acid secretion in health and disease. A better understanding of the pathways and mechanisms regulating acid secretion should lead to improved management of patients with acid-induced disorders as well as those who secrete too little acid.
Authors:
Mitchell L Schubert
Publication Detail:
Type:  Editorial; Review    
Journal Detail:
Title:  Current opinion in gastroenterology     Volume:  26     ISSN:  1531-7056     ISO Abbreviation:  Curr. Opin. Gastroenterol.     Publication Date:  2010 Nov 
Date Detail:
Created Date:  2010-10-15     Completed Date:  2011-01-28     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8506887     Medline TA:  Curr Opin Gastroenterol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  598-603     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Adenosine Triphosphatases / metabolism
Animals
Gastric Acid / metabolism,  secretion*
Gastric Mucosa / secretion*
Humans
Ion Channels
Parietal Cells, Gastric / metabolism,  secretion*
Proton Pump Inhibitors / adverse effects
Signal Transduction
Stimulation, Chemical
Chemical
Reg. No./Substance:
0/Ion Channels; 0/Proton Pump Inhibitors; EC 3.6.1.-/Adenosine Triphosphatases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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