Sulfonylurea compounds uncouple the glucose dependence of the insulinotropic effect of glucagon-like peptide 1.
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Glucagon-like peptide (GLP)-1 mimetics have been reported to cause hypoglycemia when combined with sulfonylureas. This study investigated the impact of tolbutamide on the glucose dependence of the GLP-1–mediated effects on insulin, glucagon, and somatostatin secretion in the in situ perfused rat pancreas. At 3 mmol/l glucose, GLP-1 alone did not augment insulin secretion, whereas tolbutamide alone caused a rapid increase in insulin secretion. However, when GLP-1 and tolbutamide were administered simultaneously, insulin secretion increased significantly to 43.7 ± 6.2 pmol/min (means ± SE), exceeding the sum of the responses to GLP-1 (2.0 ± 0.6 pmol/min; P = 0.019) and tolbutamide (11.3 ± 3.8; P = 0.005) alone by a factor of 3.3. At 11 mmol/l glucose, co-infusion of GLP-1 and tolbutamide augmented insulin secretion to 141.7 ± 10.3 vs. 115.36 ± 14.1 (GLP-1) and 42.5 ± 7.3 pmol/min (tolbutamide). Interestingly, increases in somatostatin secretion, both by glucose and GLP-1, were consistently paralleled by suppression of glucagon release. In conclusion, we demonstrate uncoupling of GLP-1 from its glucose dependence by tolbutamide. This uncoupling probably explains the tendency of GLP-1 to provoke hypoglycemia in combination with sulfonylureas. The results suggest that closure of ATP-sensitive K+ channels by glucose might be involved in the glucose dependence of GLP-1’s insulinotropic effect and that somatostatin acts as a paracrine regulator of glucagon release.
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These drugs can increase the risk of hypoglycemia when used with an insulin secretagogue or insulin.
“However, these drugs can increase the risk of hypoglycemia when used with an insulin secretagogue (see Ref. 88) or insulin.”
From Evaluation and Management of Adult Hypoglycemic Disorders: An Endocrine Society Clinical Practice Guideline (2009) · cites this paper as [88]
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- Authors
- de Heer, J., & Holst, J. J.
- Affiliations
- From the Department of Medical Physiology, The Panum Institute, University of Copenhagen, Copenhagen, Denmark
- University of Copenhagen (DK)
- ORCID
- Holst, Jens J.
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2007-02-01
- Volume
- 56
- Issue
- 2
- Pages
- 438-443
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2157551948
- Semantic Scholar
- 92c88b6d8a23d70735c485755165db7ac02a3470
- Cited by
- 115
- References
- 53
- Citations by year
- 2026: 3 · 2025: 4 · 2024: 4 · 2023: 5 · 2022: 2 · 2021: 4 · 2020: 4 · 2019: 7 · 2018: 3 · 2017: 5 · 2016: 6 · 2015: 5 · 2014: 6 · 2013: 8 · 2012: 8
- FWCI
- 8.30
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (submittedVersion)
- Funders
- Sundhed og Sygdom, Det Frie Forskningsråd
- European Foundation for the Study of Diabetes
- Deutsche Forschungsgemeinschaft
- Medical Research Council
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
- Keywords
- glucagon-like peptide-1, sulfonylureas, tolbutamide, insulin secretion, glucose dependence, hypoglycemia, glucagon, somatostatin, ATP-sensitive potassium channels, pancreatic islets, paracrine regulation
- MeSH terms
- Insulin Secretion, Animals, Dose-Response Relationship, Drug, Drug Therapy, Combination, Glucagon, Glucose, Hypoglycemic Agents, Insulin, Male, Somatostatin, Tolbutamide, Potassium Channels, Rats, Wistar, Rats, Glucagon-Like Peptide 1
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