Effect of Maternal Dexamethasone Treatment and Ambient Temperature on Prolactin Receptor Abundance in Brown Adipose and Hepatic Tissue in the Foetus and New‐born Lamb

Abstract

We investigated the influence of maternal dexamethasone treatment and ambient temperature on prolactin receptor (PRLR) abundance in brown adipose tissue (BAT) and hepatic tissue from foetuses and 6‐h‐old lambs delivered by caesarean section. Lambs were either delivered into a warm (30 °C; WD) or cool (15 °C; CD) ambient temperature at 140 days gestation, 2 days after dexamethasone treatment, or at 146 days gestation for controls. Uncoupling protein‐1 (UCP1) content of BAT was higher in dexamethasone‐treated groups compared to controls. A range of tissue‐specific PRLR isoforms was detected. For the long form of PRLR in BAT these isoforms had molecular weights of 66, 54, 34 and 19 kD compared with 88, 76, 66, 58, 54 and 48 kD in liver. In BAT, isoforms of the short form of PRLR had molecular weights of 66, 62, 54, 48, 33 and 31 kD compared with 82, 66, 56, 54, 48, 40 and 33 kD in liver. Dexamethasone treatment in CD lambs resulted in higher abundance of the 54 kD isoform of the short form of PRLR in liver, whilst in BAT dexamethasone resulted in a greater abundance of the 48 kD isoform of the short form, and lower abundance of the 66 kD isoform of the long form of PRLR, compared to controls. A negative correlation (r 2=0.52) was observed between abundance of 66 kD isoform for the long form of PRLR and UCP1, compared with positive correlations (r 2=0.58–0.60) for the abundance of the 54 and 48 kD isoforms for the short form of PRLR and UCP1. In conclusion, maternal dexamethasone treatment 1 week before term alters the abundance of PRLR isoforms in a tissue‐specific manner. This response is dependent on ambient temperature after birth and may provide a critical endocrine signal for maximising non‐shivering thermogenesis.