Document Detail


Gastric bypass surgery enhances glucagon-like peptide 1-stimulated postprandial insulin secretion in humans.
MedLine Citation:
PMID:  21868791     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: Gastric bypass (GB) surgery is associated with postprandial hyperinsulinemia, and this effect is accentuated in postsurgical patients who develop recurrent hypoglycemia. Plasma levels of the incretin glucagon-like peptide 1 (GLP-1) are dramatically increased after GB, suggesting that its action contributes to alteration in postprandial glucose regulation. The aim of this study was to establish the role of GLP-1 on insulin secretion in patients with GB.
RESEARCH DESIGN AND METHODS: Twelve asymptomatic individuals with previous GB (Asym-GB), 10 matched healthy nonoperated control subjects, and 12 patients with recurrent hypoglycemia after GB (Hypo-GB) had pre- and postprandial hormone levels and insulin secretion rates (ISR) measured during a hyperglycemic clamp with either GLP-1 receptor blockade with exendin-(9-39) or saline.
RESULTS: Blocking the action of GLP-1 suppressed postprandial ISR to a larger extent in Asym-GB individuals versus control subjects (33 ± 4 vs.16 ± 5%; P = 0.04). In Hypo-GB patients, GLP-1 accounted for 43 ± 4% of postprandial ISR, which was not significantly higher than that in Asym-GB subjects (P = 0.20). Glucagon was suppressed similarly by hyperglycemia in all groups but rose significantly after the meal in surgical individuals but remained suppressed in nonsurgical subjects. GLP-1 receptor blockade increased postprandial glucagon in both surgical groups.
CONCLUSIONS: Increased GLP-1-stimulated insulin secretion contributes significantly to hyperinsulinism in GB subjects. However, the exaggerated effect of GLP-1 on postprandial insulin secretion in surgical subjects is not significantly different in those with and without recurrent hypoglycemia.
Authors:
Marzieh Salehi; Ronald L Prigeon; David A D'Alessio
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Diabetes     Volume:  60     ISSN:  1939-327X     ISO Abbreviation:  Diabetes     Publication Date:  2011 Sep 
Date Detail:
Created Date:  2011-08-26     Completed Date:  2011-10-31     Revised Date:  2012-05-15    
Medline Journal Info:
Nlm Unique ID:  0372763     Medline TA:  Diabetes     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2308-14     Citation Subset:  AIM; IM    
Affiliation:
Department of Medicine, Division of Endocrinology, University of Cincinnati, Cincinnati, Ohio, USA. salehim@uc.edu
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MeSH Terms
Descriptor/Qualifier:
Adult
Blood Glucose
Female
Gastric Bypass*
Glucagon / blood
Glucagon-Like Peptide 1 / blood,  pharmacology*
Humans
Insulin / blood,  secretion*
Male
Middle Aged
Pancreas / drug effects,  secretion*
Postprandial Period / physiology*
Grant Support
ID/Acronym/Agency:
DK083554/DK/NIDDK NIH HHS; DK57900/DK/NIDDK NIH HHS; R01 DK057900/DK/NIDDK NIH HHS; UL1RR026314/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Blood Glucose; 0/Insulin; 89750-14-1/Glucagon-Like Peptide 1; 9007-92-5/Glucagon
Comments/Corrections
Comment In:
Diabetes. 2011 Sep;60(9):2203-5   [PMID:  21868790 ]

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


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