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Glucagon-like peptide 1 has a physiological role in the control of postprandial glucose in humans: studies with the antagonist exendin 9-39.
Abstract
Glucagon-like peptide 1(7-36) amide (GLP-1) is postulated to be the major physiological incretin in humans, but evidence is indirect. We report the first studies examining the physiological role of GLP-1 in the postprandial state in humans using the GLP-1 antagonist exendin 9-39. Exendin 9-39 completely blocked GLP-1-induced glucose-stimulated insulin release from perifused human islets of Langerhans. In healthy fasted volunteers, intravenous infusion of exendin 9-39 at 500 pmol x kg(-1) x min(-1) in the hyperglycemic state abolished the insulinotropic effect of a physiological dose of GLP-1 and fully reversed the glucose-lowering effect of GLP-1. Nine healthy subjects consumed a 150-g oral glucose tolerance test and were infused with 500 pmol x kg(-1) x min(-1) exendin 9-39 or saline. Exendin 9-39 increased the peak postprandial glucose level (exendin 9-39, 8.67 +/- 0.35 vs. saline, 7.67 +/- 0.35 mmol/l, P < or = 0.005) and increased postprandial plasma glucose incremental area under the curve by 35% (exendin 9-39, 152 +/- 19 vs. saline, 113 +/- 16 mmol x min x l(-1), P < or = 0.05). This could be explained as partly secondary to the blockade of glucose-induced suppression of glucagon and maybe also to an increased rate of gastric emptying. Thus, in humans exendin 9-39 acts as an antagonist of GLP-1 both in vitro and in vivo. When infused alone, exendin 9-39 causes a deterioration in postprandial glycemic control, suggesting that GLP-1 may be important for maintenance of normal postprandial glucose homeostasis in humans.
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“This peptide is known to impair oral glucose tolerance, resulting in a greater glucose AUC compared to saline (8).”
From Assessment of the incretin effect in healthy subjects: concordance between clamp and OGTT methods (2023) · cites this paper as [8]
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Harnessing the Therapeutic Potential of Glucagon-Like Peptide-1
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“[19] Administration of the GLP-1 receptor antagonist exendin[9-39] reduces the insulinotropic and glucagonostatic effects of GLP-1 and increases postprandial plasma glucose levels in vivo.”
BackgroundDhanvantari, S., Izzo, A. A., Jansen, E., & Brubaker, P. L. (2001) · Endocrinology · doi:10.1210/endo.142.1.7870 · Cited by 38
“Furthermore, the essential role of GLP-1 in the metabolic response to glucose administration has been established by studies demonstrating that acute administration of a GLP-1 antagonist leads to an increase in blood glucose levels in humans (5, 6), whereas disruption of the GLP-1 receptor in mice through homologous r…”
BackgroundExenatide can reduce glucose independent of islet hormones or gastric emptying
Ionut, V., Zheng, D., Stefanovski, D., & Bergman, R. N. (2008) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.90222.2008 · Cited by 35
Postprandial Insulin Secretion After Gastric Bypass Surgery
Holst, J. J. (2011) · Diabetes · doi:10.2337/db11-0798 · Cited by 35
“Exendin-(9-39) is an inverse agonist of the murine glucagon-like peptide-1 receptor: implications for basal in-”
Regulation of Mouse Intestinal L Cell Progenitors Proliferation by the Glucagon Family of Peptides
Grigoryan, M., Kedees, M. H., Charron, M. J., Guz, Y., & Teitelman, G. (2012) · Endocrinology · doi:10.1210/en.2012-1120 · Cited by 34
Microbiota-Produced N-Formyl Peptide fMLF Promotes Obesity-Induced Glucose Intolerance
Wollam, J., Riopel, M., Xu, Y., Johnson, A. M. F., Ofrecio, J. M., Ying, W., Ouarrat, D. E., Chan, L. S., Han, A., Mahmood, N., et al. (2019) · Diabetes · doi:10.2337/db18-1307 · Cited by 36
“To determine whether the glucose-tolerant phenotype of HFD Fpr1-KO mice is dependent upon GLP-1, we pretreated WT and Fpr1-KO HFD mice with the Glp1r antagonist exendin 9-39 (45).”
MethodPancreatic β-cell heterogeneity in adult human islets and stem cell-derived islets
Aldous, N., Moin, A. S. M., & Abdelalim, E. M. (2023) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-023-04815-7 · Cited by 40
Witte, A.-B., Grybäck, P., Jacobsson, H., Näslund, E. B., Hellström, P. M., Holst, J. J., Hilsted, L., & Schmidt, P. T. (2010) · Scandinavian Journal of Gastroenterology · doi:10.3109/00365521.2010.537680 · Cited by 34
To be or not to be—an incretin or enterogastrone?
Horowitz, M., & Nauck, M. A. (2006) · Gut · doi:10.1136/gut.2005.071787 · Cited by 33
GLP-1-induced alterations in the glucose-stimulated insulin secretory dose-response curve
Brandt, A., Katschinski, M., Arnold, R., Polonsky, K. S., Göke, B., & Byrne, M. M. (2001) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.2001.281.2.e242 · Cited by 32
“It thereby plays a physiological role in the control of postprandial glucose levels (8).”
BackgroundPACAP contributes to insulin secretion after gastric glucose gavage in mice
Filipsson, K., Holst, J. J., & Åhrén, B. (2000) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.2000.279.2.r424 · Cited by 32
“It also has been shown previously that the peptide inhibits the insulin response to oral glucose in humans (15), which supports the role of GLP-1 as an incretin hormone.”
BackgroundDemirbilek, H., Rahman, S. A., Büyükyılmaz, G., & Hussain, K. (2017) · International Journal of Pediatric Endocrinology · doi:10.1186/s13633-017-0048-8 · Cited by 35
“Exendin-(9–39) is a specific GLP-1 receptor antagonist in mice and humans [156, 157].”
BackgroundGlucagon-like peptide 1 (GLP-1) and metabolic diseases
Rotella, C. M., Pala, L., & Mannucci, E. (2005) · Journal of Endocrinological Investigation · doi:10.1007/bf03347560 · Cited by 31
Haugaard, S. B., Andersen, O., Dela, F., Holst, J. J., Storgaard, H., Fenger, M., Iversen, J., & Madsbad, S. (2005) · European Journal of Endocrinology · doi:10.1530/eje.1.01835 · Cited by 31
“A defect in the incretin signalling may also explain the b-cell dysfunction ( 47 ).”
BackgroundHypothalamic peptides as drug targets for obesity
Dhillo, W. S. (2001) · Current Opinion in Pharmacology · doi:10.1016/s1471-4892(01)00110-2 · Cited by 30
Calabria, A. C., Charles, L., Givler, S., & León, D. D. D. (2015) · Hormone Research in Paediatrics · doi:10.1159/000442155 · Cited by 30
Miller, A., Deane, A. M., Plummer, M. P., Cousins, C. E., Chapple, L. S., Horowitz, M., & Chapman, M. J. (2017) · Critical Care and Resuscitation · doi:10.1016/s1441-2772(23)00742-1 · Cited by 30
Svensson, A. M., Östenson, C., Efendić, S., & Jansson, L. E. (2007) · Clinical Science · doi:10.1042/cs20060272 · Cited by 30
Chowdhury, S., Reeds, D. N., Crimmins, D. L., Patterson, B. W., Laciny, E., Wang, S., Tran, H. D., Griest, T. A., Rometo, D. A., Dunai, J., et al. (2013) · American Journal of Physiology-Gastrointestinal and Liver Physiology · doi:10.1152/ajpgi.00383.2013 · Cited by 28
Green, B., Irwin, N., Gault, V. A., Bailey, C. J., O'Harte, F. P. M., & Flatt, P. R. (2005) · Journal of Endocrinology · doi:10.1677/joe.1.05876 · Cited by 29
“These results corroborated the findings of earlier investigations (Kolligs et al. 1995, Schirra et al. 1998, Edwards et al. 1999, Tseng et al. 1999, Green et al. 2004).”
BackgroundResultInfluential
Metadata
- Authors
- Edwards, C. M., Todd, J. F., Mahmoudi, M., Wang, Z., Wang, R. M., Ghatei, M. A., & Bloom, S. R.
- Affiliations
- Hammersmith Hospital (GB)
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 1999-01-01
- Volume
- 48
- Issue
- 1
- Pages
- 86-93
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2146581079
- Cited by
- 344
- References
- 0
- Citations by year
- 2026: 4 · 2025: 7 · 2024: 7 · 2023: 10 · 2022: 7 · 2021: 8 · 2020: 9 · 2019: 17 · 2018: 12 · 2017: 12 · 2016: 16 · 2015: 16 · 2014: 13 · 2013: 19 · 2012: 8
- FWCI
- 9.68
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Wellcome Trust
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
- Keywords
- glucagon-like peptide-1, exendin-9-39, incretins, postprandial blood glucose, glucose-stimulated insulin secretion, pancreatic islets, glucagon suppression, gastric emptying, glucose tolerance, insulinotropic effect
- MeSH terms
- Insulin Secretion, Eating, Glucagon, Glucose, Glucose Tolerance Test, Humans, Insulin, Islets of Langerhans, Peptide Fragments, Protein Precursors, Cytokines, Glucagon-Like Peptide 1, In Vitro Techniques
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