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Centre for Reproduction and Early Life, Institute of Clinical Research, Queen’s Medical Centre, University Hospital, Nottingham, NG7 2UH, UK
¹ Division of Agricultural Sciences, School of Biosciences, University of Nottingham, Sutton Bonington Campus, Loughborough, LE12 5RD, UK
² Division of Biochemical and Musculoskeletal Medicine, Human Metabolism and Clinical Biochemistry, University of Sheffield Medical School, Sheffield S10 2RX, UK
³ Division of Biomedical Sciences, University of California, Riverside, California, 92521, USA

(Requests for offprints should be addressed to H Budge, Academic Division of Child Health, Queen’s Medical Centre, University Hospital, Nottingham NG7 2UH, UK; Email: Helen.Budge{at}nottingham.ac.uk)

A primary role of the prolactin receptor (PRLR) during fetal and postnatal development has been suggested to be the regulation of uncoupling protein (UCP) expression. We, therefore, determined whether: (1) the rate of loss of UCP1 from brown adipose tissue after birth was paralleled by the disappearance of PRLR; and (2) administration of either pituitary extract prolactin (PRL) containing a mixture of posttranslationally modified forms or its pseudophosphorylated form (S179D PRL) improved thermoregulation and UCP1 function over the first week of neonatal life. PRLR abundance was greatest in adipose tissue 6 h after birth before declining up to 30 days of age, a trend mirrored by first a gain and then a loss of UCP1. In contrast, in the liver – which does not possess UCPs –a postnatal decline in PRLR was not observed. Administration of PRL resulted in an acute increase in colonic temperature in conjunction with increased plasma concentrations of non-esterified fatty acids and, as a result, the normal postnatal decline in body temperature was delayed. S179D PRL at lower concentrations resulted in a transient rise in colonic temperature at both 2 and 6 days of age. In conclusion, we have demonstrated a close relationship between the ontogeny of UCP1 and the PRLR. Exogenous PRL administration elicits a thermogenic effect suggesting an important role for the PRLR in regulating UCP1 function.

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