Format

Send to

Choose Destination
See comment in PubMed Commons below
J Clin Endocrinol Metab. 2012 Feb;97(2):589-98. doi: 10.1210/jc.2011-2561. Epub 2011 Nov 16.

Defects in GLP-1 response to an oral challenge do not play a significant role in the pathogenesis of prediabetes.

Author information

  • 1Division of Endocrinology, Mayo Clinic, Rochester, Minnesota 55905, USA.

Abstract

CONTEXT:

There has been much speculation as to whether defects in glucagon-like peptide-1 (GLP-1) secretion play a role in the pathogenesis of type 2 diabetes and the progression from normal glucose tolerance to prediabetes and diabetes.

OBJECTIVE:

Our objective was to determine whether fasting and postchallenge concentrations of active and total GLP-1 decrease as glucose tolerance and insulin secretion worsen across the spectrum of prediabetes.

DESIGN:

This was a cross-sectional study.

SETTING:

The study was performed in the clinical research unit of an academic medical center.

PARTICIPANTS:

Participants included 165 subjects with a fasting glucose below 7.0 mmol/liter and not taking medications known to affect gastrointestinal motility or glucose metabolism.

INTERVENTION:

Intervention included a 2-h, 75-g oral glucose tolerance test with insulin, C-peptide, glucagon, and GLP-1 measurements at seven time points.

MAIN OUTCOME MEASURE:

We evaluated the association of integrated, incremental active, and total GLP-1 concentrations with integrated, incremental glucose response to 75 g oral glucose.

RESULTS:

After accounting for covariates, there was no evidence of a relationship of incremental glucose concentrations after oral glucose tolerance test with active and total GLP-1 (r(s) = -0.16 and P = 0.14, and r(s) = 0.00 and P > 0.9, respectively). There also was no association of GLP-1 concentrations with insulin secretion and action.

CONCLUSIONS:

The lack of association of GLP-1 concentrations with glucose tolerance status and with insulin secretion and action in a cohort encompassing the full spectrum of prediabetes strongly argues against a significant contribution of defects in GLP-1 secretion to the pathogenesis of prediabetes.

PMID:
22090278
PMCID:
PMC3275363
DOI:
10.1210/jc.2011-2561
[PubMed - indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Silverchair Information Systems Icon for PubMed Central
    Loading ...
    Support Center