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Impact of incretin hormones on beta-cell function in subjects with normal or impaired glucose tolerance.
| Content Provider | Semantic Scholar |
|---|---|
| Author | Muscelli, Elza O. Mari, Andrea Natali, A. Astiarraga, Brenno Domingues Camastra, Stefania Frascerra, Silvia Holst, Jens Juul Ferrannini, Ele |
| Copyright Year | 2006 |
| Abstract | The mechanisms by which the enteroinsular axis influences beta-cell function have not been investigated in detail. We performed oral and isoglycemic intravenous (IV) glucose administration in subjects with normal (NGT; n = 11) or impaired glucose tolerance (IGT; n = 10), using C-peptide deconvolution to calculate insulin secretion rates and mathematical modeling to quantitate beta-cell function. The incretin effect was taken to be the ratio of oral to IV responses. In NGT, incretin-mediated insulin release [oral glucose tolerance test (OGTT)/IV ratio = 1.59 +/- 0.18, P = 0.004] amounted to 18 +/- 2 nmol/m(2) (32 +/- 4% of oral response), and its time course matched that of total insulin secretion. The beta-cell glucose sensitivity (OGTT/IV ratio = 1.52 +/- 0.26, P = 0.02), rate sensitivity (response to glucose rate of change, OGTT/IV ratio = 2.22 +/- 0.37, P = 0.06), and glucose-independent potentiation were markedly higher with oral than IV glucose. In IGT, beta-cell glucose sensitivity (75 +/- 14 vs. 156 +/- 28 pmol.min(-1).m(-2).mM(-1) of NGT, P = 0.01) and potentiation were impaired on the OGTT. The incretin effect was not significantly different from NGT in terms of plasma glucagon-like peptide 1 and glucose-dependent insulinotropic polypeptide responses, total insulin secretion, and enhancement of beta-cell glucose sensitivity (OGTT/IV ratio = 1.73 +/- 0.24, P = NS vs. NGT). However, the time courses of incretin-mediated insulin secretion and potentiation were altered, with a predominance of glucose-induced vs. incretin-mediated stimulation. We conclude that, under physiological circumstances, incretin-mediated stimulation of insulin secretion results from an enhancement of all dynamic aspects of beta-cell function, particularly beta-cell glucose sensitivity. In IGT, beta-cell function is inherently impaired, whereas the incretin effect is only partially affected. |
| Starting Page | 5 |
| Ending Page | 8 |
| Page Count | 4 |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | http://ajpendo.physiology.org/content/ajpendo/291/6/e1144.full.pdf |
| PubMed reference number | 16478775v1 |
| Volume Number | 291 |
| Issue Number | 6 |
| Journal | American journal of physiology. Endocrinology and metabolism |
| Language | English |
| Access Restriction | Open |
| Subject Keyword | Axis vertebra Beta-cell Function Measurement Cell physiology GCG gene GIP gene Glucagon-Like Peptides Immune Tolerance Impaired glucose tolerance Incretins Mathematical Concepts Mathematics Nanomole Oral Glucose Tolerance Test Polypeptides chemosensitization/potentiation insulin secretion |
| Content Type | Text |
| Resource Type | Article |
