Prokineticin 2 is involved in the thermoregulation and energy expenditure

Regul Pept. 2012 Nov 10;179(1-3):84-90. doi: 10.1016/j.regpep.2012.08.003. Epub 2012 Sep 4.

Abstract

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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptation, Physiological
  • Animals
  • Base Sequence
  • Body Temperature Regulation*
  • Body Weight / drug effects
  • Deoxyglucose / pharmacology*
  • Electroencephalography / methods
  • Energy Intake / physiology
  • Energy Metabolism*
  • Fasting / physiology
  • Female
  • Food Deprivation
  • Gastrointestinal Hormones / genetics
  • Gastrointestinal Hormones / metabolism*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Neuropeptides / genetics
  • Neuropeptides / metabolism*
  • Oxygen / metabolism
  • Paraventricular Hypothalamic Nucleus
  • Phenotype

Substances

  • Gastrointestinal Hormones
  • Neuropeptides
  • Prok2 protein, mouse
  • Deoxyglucose
  • Oxygen