期刊
DIABETES
卷 60, 期 9, 页码 2308-2314出版社
AMER DIABETES ASSOC
DOI: 10.2337/db11-0203
关键词
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资金
- American Heart Association [0635181N]
- American Society for Metabolic and Bariatric Surgery
- National Institutes of Health (NE) [DK083554, DK57900]
- National Center for Research Resources
- NUL
- Medical Research Service of the U.S. Department of Veterans Affairs
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. Diabetes 60:2308-2314, 2011
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