The Effects of Glucagon on Hepatic Metabolism
Official 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).
Study Design
- Study Type: INTERVENTIONAL
- Allocation: NON_RANDOMIZED
- Model: PARALLEL
- Masking: NONE
- Enrollment: 21 participants
Interventions
- DRUG: Glucagon response study — Please see information in group descriptions
Primary Outcomes
- Rate of Amino acid catabolism in the presence / absence of glucagon (240 minutes of study)
Secondary Outcomes
- Effect of Diabetes on amino-acid catabolism (240 minutes of study)
Trial Locations
- Mayo Clinic in Rochester, Rochester, Minnesota, United States
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AI-generated analysis for educational purposes only. This is not medical advice. Discuss clinical trial participation with your doctor. Data sourced from ClinicalTrials.gov.