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Impaired circulating glucagon-like peptide-1 response to oral glucose in women with previous gestational diabetes.

Abstract：

BACKGROUND AND OBJECTIVE:Women with previous gestational diabetes (pGDM) are at risk of developing Type 2 diabetes. Glucagon-like peptide-1 (GLP-1) potentiates the insulin response to oral glucose, and its secretion is diminished in Type 2 diabetes. The aim of the study was to see if decreased GLP-1 secretion might be an early abnormality in the progression to Type 2 diabetes and would therefore be diminished in women with pGDM. PATIENTS AND METHODS:Eleven women with pGDM and previously documented normal glucose tolerance and 11 control women underwent a 75 g oral glucose tolerance test (OGTT). Circulating plasma glucose, insulin, nonesterified fatty acids (NEFA) and GLP-1 concentrations were sampled. RESULTS:One of the women with pGDM had impaired glucose tolerance and was excluded from the study. All other women had normal glucose tolerance. The women with pGDM had higher fasting glucose concentrations than controls (5.1; 4.9-5.3 vs. 4.8; 4.4-5.1 mmol/l, median; interquartile range, P = 0.04) and greater circulating glucose area under the curve (AUC) following the oral glucose load (930; 818-1015 vs. 668; 584-737 min x mmol/l, P = 0.0007). Fasting insulin concentrations and total insulin AUC were similar. The initial (0-30 min) insulin response was decreased in the pGDM women (AUC 3981; 2783-4795 vs. 6167; 5009-8145 min x pmol/l, P = 0.05). The initial (0-30 min) GLP-1 response was reduced in the pGDM women (AUC 816; 663-984 vs. 1163; 872-2024 min x pmol/l, P = 0.02). CONCLUSION:A reduced initial GLP-1 response to oral glucose may therefore be an early abnormality in the progression to Type 2 diabetes.

journal_name

Clin Endocrinol (Oxf)

journal_title

Clinical endocrinology

authors

Forbes S,Moonan M,Robinson S,Anyaoku V,Patterson M,Murphy KG,Ghatei MA,Bloom SR,Johnston DG

doi

10.1111/j.1365-2265.2004.02172.x

keywords:

subject

Has Abstract

pub_date

2005-01-01 00:00:00

pages

51-5

issue

1

eissn

0300-0664

issn

1365-2265

pii

CEN2172

journal_volume

62

pub_type

杂志文章

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