Introduction: Prolactin (PRL) acting through its receptor may play a role in regulating fetal BAT development. Chronic administration of prolactin to the dam throughout pregnancy enhances the maturation of BAT with the resulting offspring having more UCP-1 suggesting a direct role in switching on UCP1 at birth. The present study aimed to determine the effect of PRL on UCP-1 expression postnatally.
Methods: Twenty seven female and twenty four male rats were entered into the study and randomly assigned to control (no PRL) or PRL treatment. Treatment commenced on either day 15, 30 or 60 days after birth and continued for five days. All rats were then humanely euthanased and intrascapular adipose tissue dissected and snap frozen in liquid nitrogen. UCP-1 abundance was determined in the mitochondria by immunoblotting and results expressed as a percentage of a reference sample included on all gels.
Results: PRL administration had no effect on UCP-1 abundance in male rats, or in female rats up to 15 days of age. After this age PRL treatment resulted in a marked loss (P<0.05) of UCP-1 in females. This response was not apparent in males for which the amount of UCP-1 decreased (P<0.05) between 15 and 35 days of age and therefore had less UCP-1 than age matched, untreated females.
Conclusion: Chronic PRL administration has no effect on UCP1 abundance in male rats or in females rats at 15 days of age. After 30 days of age PRL results in reduced UCP1 in female rats only. This different response according to gender may reflect differences in endogenous PRL secretion and/or PRL receptor abundance.
S.Pearce was supported by a BBSRC studentship
03 - 04 Dec 2001
Society for Endocrinology