Phase 1
N=10
The Effect of Glucagon on Rates of Hepatic Mitochondrial Oxidation in Man Assessed by PINTA
Healthy Participants
Bottom Line
View on ClinicalTrials.gov: NCT03965130 ↗Enrolled (actual)
10
Serious AEs
0.0%
Results posted
Nov 2024
Primary outcome: Primary: Rates of Hepatic Mitochondrial Oxidation — 262; 149 micromol/min
Study Design & Population
- Study type
- Interventional
- Phase
- Phase 1
- Interventions
- Glucagon (Biological); Control Study (Other)
- Age
- Adult, Older Adult · 21+ yrs
- Sex
- All
- Sponsor
- Yale University
- Primary completion
- Jul 2022
Outcome Measures
| Outcome | Result | p-value |
|---|---|---|
| PRIMARY Rates of Hepatic Mitochondrial Oxidation |
262; 149 | — |
Summary
It is well established that alterations in the portal vein insulin:glucagon ratio play a major role in the dysregulated hepatic glucose metabolism in type 2 diabetes but the molecular mechanism by which glucagon promotes alterations in hepatic glucose production and mitochondrial oxidation remain poorly understood. This is borne out of the fact that both glucagon agonists and antagonists are being developed to treat type 2 diabetes with unclear mechanisms of action.
This study will directly assess rates of mitochondrial oxidation and pyruvate carboxylase flux for the first time in humans using PINTA analysis as well as the effects of glucagon. The results will have important implications for the possibility of intervening in the pathogenesis of non alcoholic fatty liver and type 2 diabetes via chronic dual GLP-1/glucagon receptor antagonism and provide an important rationale for why a dual agonist may be more efficacious for treatment of non alcoholic fatty liver and T2D than GLP-1 alone.
Eligibility Criteria
Inclusion Criteria
- Healthy
- Non smoking
- Taking no medications except birth control
Exclusion Criteria
- Any systemic or organ disease
- Smoking
- Taking any drug or medications other than birth control (women)
Data sourced from ClinicalTrials.gov (NCT03965130). Outcome figures and adverse-event rates are extracted automatically from the registry's posted results and are provided for clinician reference, not as a substitute for the primary publication.