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Updated: Jul 6, 2026

Hyperinsulinemic-euglycemic Clamps in Conscious, Unrestrained Mice
Published on: November 16, 2011
Euglycemic hyperinsulinemia differentially modulates circulating total and acylated-ghrelin in humans
M O Weickert1, C V Loeffelholz, A M Arafat
1Department of Clinical Nutrition, German Institute of Human Nutrition Potsdam-Rehbruecke, Nuthetal, Germany. m.weickert@dife.de
Moderate hyperinsulinemia and hyperinsulinemic-hyperlipidemia do not suppress acyl-ghrelin, the active form of the appetite hormone ghrelin, in humans. This suggests other factors influence post-meal ghrelin levels.
Area of Science:
- Endocrinology
- Metabolic Research
- Gastroenterology
Background:
- Ghrelin, a gut hormone, regulates appetite.
- Des-acyl ghrelin is the predominant, inactive form in circulation.
- Acyl-ghrelin, the active form, is typically suppressed after meals.
Purpose of the Study:
- To investigate the effects of hyperinsulinemic and hyperinsulinemic-hyperlipidemic clamp conditions on circulating acyl-ghrelin levels.
- To compare responses of total ghrelin, acyl-ghrelin, and des-acyl ghrelin under these conditions.
Main Methods:
- Two-stepped euglycemic-hyperinsulinemic clamps in 14 healthy subjects.
- Inclusion of a 300-minute lipid/heparin infusion in the second step.
- Measurement of total ghrelin and acyl-ghrelin at timed intervals; des-acyl ghrelin calculated by subtraction.
Main Results:
- Total ghrelin and des-acyl ghrelin significantly decreased during both clamp conditions.
- Acyl-ghrelin levels remained unchanged from baseline throughout the clamps.
- Neither hyperinsulinemia nor hyperinsulinemic-hyperlipidemia suppressed circulating acyl-ghrelin.
Conclusions:
- Moderate hyperinsulinemia and hyperinsulinemic-hyperlipidemia do not suppress circulating acyl-ghrelin in humans.
- Factors beyond insulin and lipid levels likely mediate the post-prandial reduction of acyl-ghrelin.
- This study differentiates the regulation of total vs. active ghrelin forms.
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