Prokineticin 2 is involved in the thermoregulation and energy expenditure

被引:26
作者
Zhou, Wenbai [2 ,3 ]
Li, Jia-Da [1 ,2 ]
Hu, Wang-Ping [2 ,4 ]
Cheng, Michelle Y. [2 ]
Zhou, Qun-Yong [2 ]
机构
[1] Cent S Univ China, State Key Lab Med Genet, Changsha 410078, Hunan, Peoples R China
[2] Univ Calif Irvine, Dept Pharmacol, Irvine, CA 92697 USA
[3] Huashan Hosp, Dept Endocrinol & Metab, Shanghai, Peoples R China
[4] Xianning Coll, Dept Pharmacol, Xianning, Hubei, Peoples R China
基金
中国国家自然科学基金;
关键词
Prokineticin; 2; Torpor; Fasting; Arousal; PROTEIN-COUPLED RECEPTORS; CIRCADIAN-RHYTHMS; SUPRACHIASMATIC NUCLEUS; MICE; MOUSE; IDENTIFICATION; EXPRESSION; TORPOR; CLOCK; TEMPERATURE;
D O I
10.1016/j.regpep.2012.08.003
中图分类号
R5 [内科学];
学科分类号
100201 [内科学];
摘要
Animals have developed adaptive strategies to survive tough situations such as food shortage. However, the underlying molecular mechanism is not fully understood. Here, we provided evidence that the regulatory peptide prokineticin 2 (PK2) played an important role in such an adaptation. The PK2 expression was rapidly induced in the hypothalamic paraventricular nucleus (PVN) after fasting, which can be mimicked by 2-deoxy-D-glucose (2-DG) injection. The fasting-induced arousal was absent in the PK2-deficient (PK2(-/-)) mice. Furthermore, PK2(-/-) mice showed less energy expenditure and body weight loss than wild-type (WT) controls upon fasting. As a result. PK2(-/-) mice entered torpor after fasting. Supply of limited food (equal to 5% of body weight) daily during fasting rescued the body weight loss and hypothermal phenotype in WT mice, but not in PK2(-/-) mice. Our study thus demonstrated PK2 as a regulator in the thermoregulation and energy expenditure. (C) 2012 Elsevier B.V. All rights reserved.
引用
收藏
页码:84 / 90
页数:7
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