Loss of prokineticin receptor 2 signaling predisposes mice to torpor.
Loss of prokineticin receptor 2 signaling predisposes mice to torpor.
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DOI:
10.1152/ajpregu.00778.2007
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发表时间:
2008-06
期刊:
影响因子:
--
通讯作者:
Ebling FJ
中科院分区:
文献类型:
--
作者:
Jethwa PH;I'Anson H;Warner A;Prosser HM;Hastings MH;Maywood ES;Ebling FJ
The genes encoding prokineticin 2 polypeptide (Prok2) and its cognate receptor (Prokr2/Gpcr73l1) are widely expressed in both the suprachiasmatic nucleus (SCN) and its hypothalamic targets, and this signaling pathway has been implicated in the circadian regulation of behavior and physiology. We have previously observed that the targeted null mutation of Prokr2 disrupts circadian co-ordination of cycles of locomotor activity and thermoregulation. We have now observed spontaneous but sporadic bouts of torpor in the majority of these transgenic mice lacking Prokr2 signaling. During these torpor bouts, which lasted for up to 8h, body temperature and locomotor activity decreased markedly. Oxygen consumption and carbon dioxide production also decreased, and there was a decrease in RQ. These spontaneous torpor bouts generally began towards the end of the dark phase or in the early light phase when the mice were maintained on a 12:12 light-dark cycle, and persisted when mice were exposed to continuous darkness. Periods of food deprivation (16-24h) induced a substantial decrease in body temperature in all mice, but the duration and depth of hypothermia was significantly greater in mice lacking Prokr2 signaling compared to heterozygous and wild-type litter mates. Likewise, when tested in metabolic cages, food deprivation produced greater decreases in oxygen consumption and carbon dioxide production in the transgenic mice than the controls. We conclude that Prokr2 signaling plays a role in the hypothalamic regulation of energy balance, and loss of this pathway results in physiological and behavioral responses normally only detected when mice are in negative energy balance.
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影响因子:
64.8
作者:
Cheng, MY;Bullock, CM;Zhou, QY
通讯作者:
Zhou, QY
DOI:
10.1016/s0167-4781(02)00546-8
发表时间:
2002-12-12
期刊:
BIOCHIMICA ET BIOPHYSICA ACTA-GENE STRUCTURE AND EXPRESSION
影响因子:
--
作者:
Soga, T;Matsumoto, SI;Furuichi, K
通讯作者:
Furuichi, K
DOI:
10.1086/physzool.52.2.30152564
发表时间:
1979-01-01
期刊:
PHYSIOLOGICAL ZOOLOGY
影响因子:
--
作者:
HUDSON, JW;SCOTT, IM
通讯作者:
SCOTT, IM
DOI:
10.1073/pnas.0508881103
发表时间:
2006-03-14
影响因子:
11.1
作者:
Matsumoto, S;Yamazaki, C;Shigeyoshi, Y
通讯作者:
Shigeyoshi, Y
影响因子:
3.2
作者:
STEINLECHNER, S;HELDMAIER, G
通讯作者:
HELDMAIER, G