Hyperinsulinemic Hypoglycemia with Nesidioblastosis after Gastric-Bypass Surgery

To the Editor: The causal links between bariatric surgery and pancreatic nesidioblastosis are unclear. Service et al. (July 21 issue) 1 suggest a link between nesidioblastosis and glucagon-like peptide 1 (GLP-1), since GLP-1 causes beta-cell expansion in animal models of diabetes. GLP-1 and the incr...

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Bibliographic Details
Published inThe New England journal of medicine Vol. 353; no. 20; pp. 2192 - 2194
Main Authors Carpenter, Thomas, Trautmann, Michael E, Baron, Alain D
Format Journal Article
LanguageEnglish
Published United States Massachusetts Medical Society 17.11.2005
Subjects
Animals
Diabetes Mellitus, Type 2 - drug therapy
Gastric Bypass - adverse effects
Glucagon-Like Peptide 1 - adverse effects
Humans
Hyperinsulinism - etiology
Hypoglycemia - etiology
Insulin-Secreting Cells - drug effects
Nesidioblastosis - etiology
Peptides - adverse effects
Peptides - therapeutic use
Postoperative Complications
Venoms - adverse effects
Venoms - therapeutic use
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Summary:To the Editor: The causal links between bariatric surgery and pancreatic nesidioblastosis are unclear. Service et al. (July 21 issue) 1 suggest a link between nesidioblastosis and glucagon-like peptide 1 (GLP-1), since GLP-1 causes beta-cell expansion in animal models of diabetes. GLP-1 and the incretin mimetic exenatide enhance insulin secretion in a glucose-dependent manner. 2 , 3 Similarly, incretin-induced beta-cell expansion appears to be glucose-dependent. It is relevant that studies of two years' duration in normal mice and rats of exenatide at doses of more than 100 times those given to humans showed no pathological changes in the islets (data on file, Amylin . . .
Bibliography:SourceType-Other Sources-1
content type line 63
ObjectType-Correspondence-1
ObjectType-Commentary-2
ISSN:0028-4793
1533-4406
DOI:10.1056/NEJM200511173532017