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dc.contributor.authorRayner, C.en
dc.contributor.authorHorowitz, M.en
dc.identifier.citationJournal of Clinical Investigation, 2006; 116(2):299-302en
dc.descriptionCopyright © 2006 by the American Society for Clinical Investigationen
dc.description.abstractUpper gastrointestinal dysfunction occurs frequently in diabetes and potentially contributes to both abdominal symptoms and impaired glycemic control; conversely, variations in blood glucose concentration reversibly affect gut motility in humans. In this issue of the JCI, Anitha et al. report apoptosis of rodent enteric neurons under hyperglycemic conditions, both in vitro and in vivo, associated with impaired PI3K activity and preventable by glial cell line–derived neurotrophic factor (see the related article beginning on page 344). These observations add to recent insights gained from animal models regarding the etiology of diabetic gastrointestinal dysfunction, but investigators must strive to translate animal data to human diabetes.en
dc.description.statementofresponsibilityChristopher K. Rayner and Michael Horowitzen
dc.publisherAmer Soc Clinical Investigation Incen
dc.subjectAnimals; Humans; Gastrointestinal Diseases; Diabetes Mellitus; Diabetes Complications; Blood Glucose; Gastrointestinal Motility; Phosphatidylinositol 3-Kinasesen
dc.titleGastrointestinal motility and glycemic control in diabetes: the chicken and the egg revisited?en
dc.typeJournal articleen
pubs.library.collectionMedicine publicationsen
dc.identifier.orcidRayner, C. [0000-0002-5527-256X]en
dc.identifier.orcidHorowitz, M. [0000-0002-0942-0306]en
Appears in Collections:Medicine publications

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