The Effects of Glucagon on Hepatic Metabolism

Completed · Phase 1/Phase 2

Conditions studied: Obesity, Type2diabetes, NAFLD

In brief

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).

Key facts

Study ID

NCT05500586

Run by

Adrian Vella

People needed

21

Starts

2022-10-20

Expected to finish

2026-03-31

Last updated by the study team

2026-04-29

Who can join

Age: 25 and older, up to 65. Sex: any. Healthy volunteers: accepted.

You may qualify if…

• Willing to participate
• Able to give consent

You may not qualify if…

• 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

Where it is running

• Mayo Clinic in Rochester — Rochester, Minnesota, United States

Full record on ClinicalTrials.gov

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