Trials / Completed
CompletedNCT04459338
A Dose-response Study Examining the Contribution of GLP-1 Receptor Signaling to Glucagon-stimulated Insulin Secretion
- Status
- Completed
- Phase
- Phase 3
- Study type
- Interventional
- Enrollment
- 11 (actual)
- Sponsor
- Adrian Vella · Academic / Other
- Sex
- All
- Age
- 25 Years – 65 Years
- Healthy volunteers
- Accepted
Summary
The GLP-1 receptor (GLP1R) gene is found on the beta cells of the pancreas. Its role is in the control of blood sugar level by enhancing insulin secretion from the pancreas after eating a meal. The purpose of this research study is to evaluate the role of GLP1R in the response to elevated glucagon concentrations.
Detailed description
Glucagon within the islet can signal the β-cell through GLP1R, and acts as an insulin secretagogue. This signaling is blocked by exendin-9,39. The relative importance of glucagon signaling through its cognate receptor or through GLP1R is unknown. Despite the lower affinity of GLP1R for glucagon, intra-islet concentrations of glucagon are sufficiently high to stimulate GLP1R. The other situation where this may occur is in response to pharmacologic doses of glucagon as used for β-cell function testing or raising peripheral glucagon concentrations above fasting values. The experiments proposed will characterize the role of GLP1R in glucagon's actions on the β-cell and the potential therapeutic role of dual (GLP-1R and glucagon receptor) agonists for the treatment of T2DM and obesity.
Conditions
Interventions
| Type | Name | Description |
|---|---|---|
| BIOLOGICAL | Exendin-9,39 | Exendin-9,39 is a competitive antagonist of GLP-1 actions at the GLP-1 receptor |
| OTHER | Saline | Placebo comparator |
Timeline
- Start date
- 2021-03-04
- Primary completion
- 2022-06-14
- Completion
- 2022-06-14
- First posted
- 2020-07-07
- Last updated
- 2023-06-09
- Results posted
- 2023-06-09
Locations
1 site across 1 country: United States
Regulatory
- FDA-regulated drug study
Source: ClinicalTrials.gov record NCT04459338. Inclusion in this directory is not an endorsement.