The Effects of Glucagon on Hepatic Metabolism

• Status: Not yet recruiting
• Trial end date: 2024-12-31
• Target enrollment: 0
• Participant gender: All

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).

• Phase: Phase 1/Phase 2
• Accepts Healthy Volunteers?: Accepts Healthy Volunteers

Details

• Lead Sponsor: Adrian Vella
• Treatments: Glucagon

Criteria

Inclusion Criteria:

• Willing to participate

• Able to give consent

Exclusion Criteria:

• History of prior upper abdominal surgery e.g. gastric banding, pyloroplasty, vagotomy.

• Active systemic illness or malignancy.

• Symptomatic macrovascular or microvascular disease.

• Contraindications to MRI (e.g. metal implants, claustrophobia).

• Hematocrit < 35%

• TSH < 0.4 or > 5.5.

• Consumption of > 2 alcohol drinks per day or > 14 per week or a positive AUDIT questionnaire