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Updated: Feb 11, 2026

Determining Basal Energy Expenditure and the Capacity of Thermogenic Adipocytes to Expend Energy in Obese Mice
06:57

Determining Basal Energy Expenditure and the Capacity of Thermogenic Adipocytes to Expend Energy in Obese Mice

Published on: November 11, 2021

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Oxyntomodulin analogue increases energy expenditure via the glucagon receptor

R Scott1, J Minnion1, T Tan1

  • 1Division of Diabetes, Endocrinology and Metabolism, Imperial College London, Hammersmith Hospital, Du Cane Road, London W12 0NN, United Kingdom.

Peptides
|April 23, 2018
PubMed

Insights

Oxyntomodulin (OXM) increases energy expenditure through glucagon receptor activation, not GLP-1 receptors. This finding is crucial for developing effective obesity treatments with dual-acting analogues.

Area of Science:

  • Metabolism and Endocrinology
  • Pharmacology
  • Obesity Research

Background:

  • Oxyntomodulin (OXM) is a gut hormone recognized for its potential in weight management by suppressing appetite and boosting energy expenditure.
  • The precise mechanisms underlying OXM's physiological effects, particularly the receptor(s) mediating increased energy expenditure, remain incompletely understood.
  • While OXM interacts with both glucagon and GLP-1 receptors, the specific receptor responsible for its thermogenic effects is debated.

Purpose of the Study:

  • To investigate the specific receptor pathways responsible for the energy expenditure effects of the sustained-release oxyntomodulin analogue, OX-SR.
  • To determine whether glucagon receptor or GLP-1 receptor activation is primarily responsible for OX-SR-induced increases in energy expenditure.
  • To provide insights for the rational design of novel obesity therapeutics targeting OXM pathways.

Main Methods:

  • Utilized indirect calorimetry in rats to measure energy expenditure following administration of OX-SR.
  • Employed receptor blockade strategies, specifically using Exendin 9-39 to inhibit GLP-1 receptor activity.
  • Assessed the impact of glucagon receptor antagonism on OX-SR-mediated energy expenditure changes.

Main Results:

  • OX-SR administration led to a significant and sustained increase in energy expenditure in rats.
  • Blocking the GLP-1 receptor with Exendin 9-39 did not attenuate the increase in oxygen consumption induced by OX-SR.
  • Inhibition of glucagon receptor activity abolished the OX-SR-stimulated increase in energy expenditure, confirming its essential role.

Conclusions:

  • Glucagon receptor activation is essential for the observed increase in energy expenditure mediated by the sustained-release oxyntomodulin analogue OX-SR.
  • The anorectic effects of OXM may involve GLP-1 receptors, but its thermogenic effects are primarily mediated via glucagon receptors.
  • Future development of dual-acting analogues for obesity treatment necessitates a careful balance of GLP-1 and glucagon receptor activities to optimize therapeutic outcomes.
Keywords:
Energy expenditureGLP-1GlucagonOxyntomodulinReceptor

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