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OpenTrials
Completed

NCT Number: NCT05500586

The Effects of Glucagon on Hepatic Metabolism

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).

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Key information

Conditions

Obesity Body Weight Digestive System Diseases Fatty Liver Glucose Metabolism Disorders Hyperinsulinism Insulin Resistance Liver Diseases Metabolic Diseases NAFLD Non-alcoholic Fatty Liver Disease Nutrition Disorders Nutritional and Metabolic Diseases Overnutrition Overweight Pathological Conditions, Signs and Symptoms Signs and Symptoms Type2diabetes

Age range

25 year–65 year

Sex eligibility

All sexes

Study type

Interventional

Phase

Phase 1 / Phase 2

Primary location

Mayo Clinic in Rochester

Rochester, Minnesota, 55905, United States

About this study

T2DM and prediabetes are characterized by abnormal post-prandial suppression of glucagon, which contributes to postprandial hyperglycemia by increasing EGP. Although these effects are magnified by decreased and delayed insulin secretion, they are also apparent when insulin secretion is intact. In rodents, altered glucagon signaling changes α-cell function and mass - an effect mediated by changes in circulating AA concentrations. Are the elevated concentrations of branched-chain AA and other AA metabolites in T2DM a cause or an effect of global α-cell dysfunction? Could altered glucagon signaling precipitate a vicious cycle resulting in T2DM?

Who can participate

Healthy volunteers accepted: Yes

Only the study team can determine whether someone qualifies for participation.

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

Treatment and study plan

Glucagon response study

Drug

Please see information in group descriptions

Other names: Glucagon

Primary outcomes

  1. Rate of Amino acid catabolism in the presence / absence of glucagon

    Time frame: 240 minutes of study

    Tracer-dependent measurement of amino-acid clearance

Secondary outcomes

  1. Effect of Diabetes on amino-acid catabolism

    Time frame: 240 minutes of study

    Tracer-dependent measurement of amino-acid clearance

Sponsors and collaborators

Lead sponsor

Adrian Vella

Other

Registry information

Important dates

Study start
2022
Primary completion
2025
Study completion
2026
First posted
Aug 15, 2022
Registry last updated
Apr 29, 2026

OpenTrials presents study information sourced from ClinicalTrials.gov. The official registry record should be consulted for the latest information.

View the official ClinicalTrials.gov record (opens in a new tab)

This listing is for discovery and informational purposes only. It is not medical advice, does not guarantee that a study is recruiting, and does not determine eligibility. Contact the study team and a qualified healthcare professional when considering participation.

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