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The Effects of Glucagon on Hepatic Metabolism

NCT05500586 · Status: COMPLETED · Phase: PHASE1/PHASE2 · Type: INTERVENTIONAL · Enrollment: 21

Last updated 2026-04-29

No results posted yet for this study

Summary

Whether impaired postprandial glucagon suppression in prediabetes and T2DM is an attempt to overcome resistance to glucagon's actions on hepatic AA catabolism, a defect in α-cell function, or a combination of both are important, unanswered questions. NAFLD is associated with T2DM risk and impaired insulin action. Unfortunately, it is unclear if glucagon resistance is caused by obesity, hepatic steatosis or both. The experiments outlined will determine if glucagon's actions on hepatic amino acid catabolism and EGP interact with hepatic lipid metabolism in lean and obese subjects with and without T2DM (and with varying degrees of hepatic steatosis).

Conditions

Interventions

DRUG

Glucagon response study

Please see information in group descriptions

Sponsors & Collaborators

  • Adrian Vella

    lead OTHER

Principal Investigators

  • Adrian Vella · Mayo Clinic

Study Design

Allocation
NON_RANDOMIZED
Purpose
BASIC_SCIENCE
Masking
NONE
Model
PARALLEL

Eligibility

Min Age
25 Years
Max Age
65 Years
Sex
ALL
Healthy Volunteers
Yes

Timeline & Regulatory

Start
2022-10-20
Primary Completion
2025-09-30
Completion
2026-03-31
FDA Drug
Yes

Countries

  • United States

Study Locations

More Related Trials

Entities

Diseases

Read the full study record

This page highlights key information. For complete eligibility criteria, study locations, investigator contacts, and the full protocol, visit the original record on ClinicalTrials.gov.

View NCT05500586 on ClinicalTrials.gov