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Estrous cycle modulates fasting-induced torpor propensity via hypothalamic estrogen signalling
Christopher J Marshall1, Anthony E Pickering2, Michael T Ambler2
1Anaesthesia, Pain and Critical Care Research, School of Physiology, Pharmacology & Neuroscience, University of Bristol, Bristol, BS8 1TD, UK. chris.marshall@bristol.ac.uk.
Estradiol levels influence the ability of mice to enter torpor, a state of reduced metabolism. Estrogen receptor alpha in the hypothalamus is key for this fasting-induced torpor response.
Area of Science:
- Physiology
- Neuroendocrinology
- Metabolic Regulation
Background:
- Torpor is a survival strategy involving reduced metabolism and body temperature during scarcity.
- The hypothalamus, specifically the preoptic area (POA), plays a role in regulating torpor.
- Estrogens, like estradiol, are known to influence energy balance and thermogenesis via central mechanisms.
Purpose of the Study:
- To investigate the role of estrogen signaling within the POA in mediating fasting-induced torpor in mice.
- To determine if estradiol modulates torpor depth, duration, and propensity.
Main Methods:
- Monitoring torpor patterns across the estrus cycle in female mice.
- Administering exogenous estradiol to male and female mice.
- Utilizing ERα (estrogen receptor alpha) knockdown in the POA of female mice.
Main Results:
- Torpor depth and duration varied with the estrus cycle, peaking during diestrus when estradiol is highest.
- Exogenous estradiol extended torpor bouts in females but not males.
- ERα knockdown in the POA significantly reduced torpor in female mice.
Conclusions:
- Estradiol signaling through ERα in the POA is crucial for regulating fasting-induced torpor in female mice.
- Cyclical variations in torpor propensity may be an adaptive mechanism to balance energy conservation and reproduction.
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