Summary
Glucose is a significant energy resource for maintaining physiological activities, including body temperature homeostasis, and glucose homeostasis is tightly regulated in mammals. Although ambient temperature tunes glucose metabolism to maintain euthermia, the significance of body temperature in metabolic regulation remains unclear owing to strict thermoregulation. Activation of Qrfp neurons in the preoptic area induced a harmless hypothermic state known as Q-neuron-induced hypothermia and hypometabolism (QIH), which is suitable for studying glucose metabolism under hypothermia. In this study, we first observed that QIH mice had hyperinsulinemia and insulin resistance. This glucose hypometabolic state was abolished by increasing the body temperature to euthermia. Moreover, QIH-mediated inappetence and locomotor inactivity were recovered in euthermia QIH mice. These results indicate that body temperature is considerably more powerful than ambient temperature in regulating glucose metabolism and behavior, and hypometabolism in QIH is secondary to hypothermia rather than modulated by Qrfp neurons.
Highlights
QIH reorganizes glucose homeostasis which is unchanged by fasting.
QIH mice exhibit glucose hypometabolism with hyperinsuliemia and insulin resistance.
Increased body temperature abolishes QIH-mediated hypometabolism and torpid behaviors.
Body temperature is a strong factor in controlling metabolism and behavior.
Body temperature-mediated glucose metabolism is reversible.
Competing Interest Statement
The authors have declared no competing interest.
Footnotes
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