Prolactin Mediates Long-Term, Seasonal Rheostatic Regulation of Body Mass in Female Mammals

Author:

Marshall Christopher J1,Blake Alexandra2,Stewart Calum3,Liddle T Adam3,Denizli Irem3,Cuthill Fallon3,Evans Neil P3,Stevenson Tyler J3ORCID

Affiliation:

1. School of Physiology, Pharmacology and Neuroscience, University of Bristol , Bristol BS8 1TD , UK

2. Institute of Molecular Biology, University of Mainz , Mainz 55122 , Germany

3. School of Biodiversity, One Health and Veterinary Medicine, University of Glasgow , Glasgow G61 1QH , UK

Abstract

Abstract A series of well-described anabolic and catabolic neuropeptides are known to provide short-term, homeostatic control of energy balance. The mechanisms that govern long-term, rheostatic control of regulated changes in energy balance are less well characterized. Using the robust and repeatable seasonal changes in body mass observed in Siberian hamsters, this report examined the role of prolactin in providing long-term rheostatic control of body mass and photoinduced changes in organ mass (ie, kidney, brown adipose tissue, uterine, and spleen). Endogenous circannual interval timing was observed after 4 months in a short photoperiod, indicated by a significant increase in body mass and prolactin mRNA expression in the pituitary gland. There was an inverse relationship between body mass and the expression of somatostatin (Sst) and cocaine- and amphetamine-regulated transcript (Cart). Pharmacological inhibition of prolactin release (via bromocriptine injection), reduced body mass of animals maintained in long photoperiods to winter–short photoperiod levels and was associated with a significant increase in hypothalamic Cart expression. Administration of ovine prolactin significantly increased body mass 24 hours after a single injection and the effect persisted after 3 consecutive daily injections. The data indicate that prolactin has pleiotropic effects on homeostatic sensors of energy balance (ie, Cart) and physiological effectors (ie, kidney, BAT). We propose that prolactin release from the pituitary gland acts as an output signal of the hypothalamic rheostat controller to regulate adaptive changes in body mass.

Funder

Leverhulme Trust Research Leader

Publisher

The Endocrine Society

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