Incretin effect potentiates β-cell responsivity to glucose as well as to its rate of change: OGTT and matched intravenous study
Abstract
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 (Φ s = 16.4 ± 1.8 vs. 24.6 ± 2.0 10−9 min−1, P = 0.01) and 63% for the dynamic (Φ 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 β-cell to glucose, these results suggest that incretins may modulate more than one step in the β-cell insulin secretory cascade.
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In Ref. 5, the difference between oral and intravenous β-cell responsivity indexes provided an indirect measure of the incretin effect; there was an approximately 60% difference between the two indexes, implying that the incretin effect is responsible for such potentiation.
“The difference between oral and intravenous indexes provided an indirect measure of the incretin effect; there was an ∼60% difference between the two indexes, implying that the incretin effect is responsible for such potentiation.”
From A model of GLP-1 action on insulin secretion in nondiabetic subjects (2010) · cites this paper as [5]
The percentage increases of Φd and Φs due to incretins were similar (58 and 63%, respectively) in Ref. 5.
“where the percentage increases of Φd and Φs due to incretins were similar (58 and 63%, respectively).”
From A model of GLP-1 action on insulin secretion in nondiabetic subjects (2010) · cites this paper as [5]
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Sucralose affects glycemic and hormonal responses to an oral glucose load
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Self-citationDalla Man, C., Micheletto, F., Sathananthan, M., Vella, A., & Cobelli, C. (2016) · Diabetes Technology & Therapeutics · doi:10.1089/dia.2015.0146 · Cited by 24 · see citing works
Self-citation
- Authors
- Campioni, M., Toffolo, G., Shuster, L. T., Service, F. J., Rizza, R. A., & Cobelli, C.
- Affiliations
- University of Padua (IT)
- Venue
- American Journal of Physiology-Endocrinology and Metabolism
- Publisher
- American Physiological Society
- Published
- 2007-01
- Volume
- 292
- Issue
- 1
- Pages
- E54-E60
- ISSN
- 0193-1849 (ISSN-L)
- 1522-1555
- OpenAlex
- W2144525814
- Cited by
- 40
- References
- 24
- Citations by year
- 2026: 1 · 2021: 2 · 2020: 1 · 2017: 3 · 2016: 1 · 2015: 1 · 2014: 5 · 2013: 4 · 2012: 3
- FWCI
- 3.73
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Physiology-Endocrinology and Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Padua Research Archive (University of Padova) (submittedVersion)
- Funders
- National Institutes of Health
- National Institute of Diabetes and Digestive and Kidney Diseases (DK 29953)
- National Center for Research Resources (RR-00585, M01RR000585)
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
- Keywords
- incretins, beta-cell insulin secretion, glucose-stimulated insulin secretion, C-peptide secretion, oral glucose tolerance test, intravenous glucose infusion, exocytosis
- MeSH terms
- Administration, Oral, Adult, Blood Glucose, C-Peptide, Female, Glucose, Glucose Tolerance Test, Humans, Injections, Intravenous, Insulin, Male, Case-Control Studies, Insulin-Secreting Cells
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