Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/9231
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dc.contributor.authorZhang, Q.en
dc.contributor.authorHorowitz, M.en
dc.contributor.authorTippett, R.en
dc.contributor.authorRayner, C.en
dc.contributor.authorWorynski, A.en
dc.contributor.authorHolloway, R.en
dc.date.issued2004en
dc.identifier.citationAmerican Journal of Physiology-Gastrointestinal and Liver Physiology, 2004; 286(5):G797-G803en
dc.identifier.issn0193-1857en
dc.identifier.issn1522-1547en
dc.identifier.urihttp://hdl.handle.net/2440/9231-
dc.description© 2005 by the American Physiological Society. Published abstract reprinted by permission of the copyright owner.en
dc.description.abstractAcute changes in blood glucose concentration have major effects on gastrointestinal motor function. Patients with diabetes mellitus have an increased prevalence of gastroesophageal reflux. Transient lower esophageal sphincter (LES) relaxation (TLESR) is the most common sphincter mechanism underlying reflux. The aim of this study was to investigate the effect of acute hyperglycemia on triggering TLESRs evoked by gastric distension in healthy volunteers. TLESRs were stimulated by pressure-controlled and volume-controlled (500 ml) gastric distension using an electronic barostat and performed on separate days. On each day, esophageal manometry was performed in the sitting position during gastric distension for 1 h under euglycemia (5 mM), and either marked hyperglycemia (15 mM) or physiological hyperglycemia (8 mM) in randomized order was maintained by a glucose clamp. Marked hyperglycemia doubled the rate of TLESRs in response to both pressure-controlled [5 (3–10.5, median or interquartile range) to 10 (9.5–14.5) per hour, P < 0.02] and volume-controlled [4 (2.5–7.5) to 10.5 (7–12.5) per hour, P < 0.02] gastric distension but had no effect on basal LES pressure. Physiological hyperglycemia had no effect on the triggering of TLESRs or basal LES pressure. In healthy human subjects, marked hyperglycemia increases the rate of TLESRs. Increase in the rate of TLESRs is independent of proximal gastric wall tension. Mechanisms underlying the effect remain to be determined. Hyperglycemia may be an important factor contributing to the increased esophageal acid exposure in patients with diabetes mellitus.en
dc.description.statementofresponsibilityQing Zhang, Michael Horowitz, Rachael Rigda, Christopher Rayner, Andrew Worynski, and Richard H. Hollowayen
dc.language.isoenen
dc.publisherAmer Physiological Socen
dc.subjectdiabetes mellitus; esophageal motility; gastroesophageal relux diseaseen
dc.titleEffect of hyperglycemia on triggering of transient lower esophageal sphincter relaxationsen
dc.typeJournal articleen
dc.identifier.rmid0020040324en
dc.identifier.doi10.1152/ajpgi.00383.2003en
dc.identifier.pubid57120-
pubs.library.collectionMedicine publicationsen
pubs.verification-statusVerifieden
pubs.publication-statusPublisheden
dc.identifier.orcidHorowitz, M. [0000-0002-0942-0306]en
dc.identifier.orcidRayner, C. [0000-0002-5527-256X]en
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