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Cold-induced hyperphagia requires AgRP neuron activation in mice
Jennifer D Deem1, Chelsea L Faber1, Christian Pedersen2
1UW Medicine Diabetes Institute, Department of Medicine, University of Washington, Seattle, United States.
Elife
|December 15, 2020
Summary
Cold exposure rapidly activates agouti-related peptide (AgRP) neurons, increasing energy intake but not expenditure. Silencing these neurons blocks cold-induced overeating, highlighting their key role in regulating appetite during cold.
Area of Science:
- Neurobiology
- Energy Homeostasis
- Metabolism
Background:
- Cold exposure increases energy demands via thermogenesis, requiring compensatory increases in energy intake.
- The neurobiological mechanisms driving cold-induced hyperphagia remain incompletely understood.
- Agouti-related peptide (AgRP) neurons are key regulators of appetite and energy balance.
Purpose of the Study:
- To investigate the role of AgRP neurons in the hyperphagic response to acute cold exposure.
- To determine if AgRP neuron activation is necessary for cold-induced increases in energy intake.
Main Methods:
- Acute cold exposure in animal models.
- Monitoring of AgRP neuron activity.
- Measurement of energy expenditure and energy intake.
- Selective silencing of AgRP neurons to assess functional necessity.
Main Results:
- AgRP neuron activation occurred rapidly upon acute cold exposure.
- Cold exposure increased both energy expenditure and energy intake.
- Silencing AgRP neurons blocked cold-induced hyperphagia but did not affect energy expenditure.
Conclusions:
- The perception of cold is sufficient to activate AgRP neurons and stimulate feeding.
- AgRP neurons play a critical and specific role in mediating the hyperphagic response to cold.
- These findings elucidate a key neural pathway for regulating energy intake in response to environmental temperature.
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