Journal
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
Volume 292, Issue 1, Pages E54-E60Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpendo.00033.2006
Keywords
oral glucose tolertance test; insulin secretion; beta-cell function; minimal model
Categories
Funding
- NCRR NIH HHS [RR-00585] Funding Source: Medline
- NIDDK NIH HHS [DK-29953] Funding Source: Medline
Ask authors/readers for more resources
The aim of this study is to gain greater insight into the mechanism whereby incretins ( greater insulinemia after oral than intravenous glucose) enhance insulin secretion. To do so, we use a model of C-peptide secretion to reanalyze data from a previously published study in which glycemic profiles observed following glucose ingestion were matched in the same 10 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(-9) min(-1), P = 0.01) and 63% for the dynamic ( Phi(d) = 278 +/- 32 vs. 463 +/- 86 10(-9), P = 0.02) indexes. 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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available