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Diabetes. 2012 Feb;61(2):447-53. doi: 10.2337/db11-0995.

Distinct β-cell defects in impaired fasting glucose and impaired glucose tolerance.

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  • 1Division of Diabetes, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA.

Abstract

To characterize the defects in β-cell function in subjects with impaired fasting glucose (IFG) and compare the results to impaired glucose tolerance (IGT) and normal glucose tolerance (NGT) subjects, β-cell glucose sensitivity and rate sensitivity during the oral glucose tolerance test were measured with the model by Mari in 172 Mexican Americans. A subgroup (n=70) received a 2-h hyperglycemic clamp (+125 mg/dL), and first- and second-phase insulin secretion were quantitated. Compared with NGT, subjects with IFG and IGT manifested a decrease in β-cell glucose sensitivity; IFG subjects, but not IGT subjects, had decreased β-cell rate sensitivity. In IFG subjects, the defect in β-cell glucose sensitivity was time dependent, began to improve after 60 min, and was comparable to NGT after 90 min. The incremental area under the plasma C-peptide concentration curve during the first 12 min of the hyperglycemic clamp (ΔC-pep[AUC]0-12) was inversely related with the increase in FPG concentration (r=-36, r=0.001), whereas ΔC-pep[AUC]15-120 positively correlated with FPG concentration (r=0.29, r<0.05). When adjusted for the prevailing level of insulin resistance, first-phase insulin secretion was markedly decreased in both IFG and IGT, whereas second-phase insulin secretion was decreased only in IGT. These results demonstrate distinct defects in β-cell function in IFG and IGT.

PMID:
22275086
[PubMed - indexed for MEDLINE]
PMCID:
PMC3266412
Free PMC Article
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