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Am J Physiol Endocrinol Metab (July 25, 2006). doi:10.1152/ajpendo.00033.2006
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Submitted on January 25, 2006
Accepted on July 24, 2006

INCRETIN EFFECT POTENTIATES BETA-CELL RESPONSIVITY TO GLUCOSE AS WELL AS TO ITS RATE OF CHANGE: OGTT AND MATCHED INTRAVENOUS STUDY

Marco Campioni1, Gianna Maria Toffolo1, LYNNE T SHUSTER2, F. John Service3, Robert A. Rizza3, and Claudio Cobelli1*

1 Department of Information Engineering, University of Padova, Padova, Italy
2 Department of Internal Medicine, Women's Health Clinic, Mayo Clinic & Foundation, Rochester, Minnesota, United States
3 Department of Internal Medicine, Division of Endocrinology, Diabetes, Metabolism & Nutrition, Mayo Clinic & Foundation, Rochester, Minnesota, United States

* To whom correspondence should be addressed. E-mail: cobelli{at}dei.unipd.it.

The aim of this study it is to gain greater insight into the mechanism by which "incretins" (greater insulinemia after oral than intravenous glucose) enhances insulin secretion. In order to do so, we use a model of C-peptide secretion to reanalyse data from a previously published study in which glycemic profiles observed following glucose ingestion were matched in the same ten subjects by means of an intravenous glucose infusion. We report that incretins increase insulin secretion by enhancing both the dynamic (to the rate of increase of glucose) and static (to given glucose concentration) response with an increase of 58% for the static ({Phi}s=16.4 ± 1.8 vs. 24.6 ± 2.0 (10-9min-1); P=0.01) and 63% for the dynamic ({Phi}d=278 ± 32 vs. 463 ± 86 (10-9); P=0.02) indices. Since increases in the dynamic response to glucose are believed to be due to an increase in the rate of docking and exocytosis of insulin containing granules and increases in the static response to glucose are believed to be caused by a shift in the sensitivity of the {beta}-cell to glucose, these results suggest that incretins may modulate more than one step in the {beta}-cell insulin secretory cascade.




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