The hyperthermic response to intra-preoptic area administration of agmatine in male rats

Xu, Jianhui; Gao, Wenmin; He, Tianhui; Yao, Ling; Wu, Hanghong; Chen, Zhenwei; Lai, Yupei; Chen, Yajun; Zhang, Jie

doi:10.1016/j.jtherbio.2023.103529

“…Although QIH mice had a markedly low heart rate, which was also noted in hypothermia induced by estrogen receptor-expressing neurons in the POA (Zhang et al, 2020), whether bradycardia is controlled by these neurons or by hypothermia needs further studies. Besides body temperature, the POA regulates locomotor activity (Brudzynski and Mogenson, 1986;Ogawa et al, 2003;Xu et al, 2023;Zhang et al, 2023). The locomotor activity of QIH mice, which was extremely inhibited at 23°C, was higher than that of the control at 34°C, suggesting that Qrfp POA activation enhanced locomotion, and this enhancement was masked by hypothermia in QIH mice (Sinnamon, 1992(Sinnamon, , 1993.…”

Section: Discussionmentioning

confidence: 99%

“…Although QIH mice had a markedly low heart rate, which was also noted in hypothermia induced by estrogen receptor-expressing neurons in the POA (Zhang et al, 2020), whether bradycardia is controlled by these neurons or by hypothermia needs further studies. Besides body temperature, the POA regulates locomotor activity (Brudzynski and Mogenson, 1986;Ogawa et al, 2003;Xu et al, 2023;Zhang et al, 2023).…”

Section: Discussionmentioning

confidence: 99%

Body temperature regulates glucose metabolism and torpid behavior

Lee,

Chang,

Toda

et al. 2024

Preprint

0

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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.

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“…Although QIH mice had a markedly low heart rate, which was also noted in hypothermia induced by estrogen receptor-expressing neurons in the POA 42 , whether bradycardia is controlled by these neurons or by hypothermia needs further studies. Besides body temperature, the POA regulates locomotor activity [43][44][45][46] . The locomotor activity of QIH mice, which was extremely inhibited at 23°C, was higher than that of the control at 34°C, suggesting that Qrfp POA activation enhanced locomotion, and this enhancement was masked by hypothermia in QIH mice 47,48 .…”

Section: Discussionmentioning

confidence: 99%

Body temperature regulates glucose metabolism and torpid behavior

Lee,

Chang,

Toda

et al. 2024

Preprint

0

View full text Add to dashboard Cite

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.

show abstract