Endocrine Abstracts (2003) 6 OC19


J Bispham, T Stephenson & ME Symonds

Academic Division of Child Health, School of Human Development, University of Nottingham, Nottingham, UK.

Introduction: Fetal fat comprises both brown and white adipocytes. Brown fat possess a unique uncoupling protein 1 (UCP1), whose abundance is regulated in part by the prolactin receptor (PRLR), whereas white fat is characterised as secreting leptin. The present study aimed to determine if the relationship between mRNA abundance for each of these molecular indices of adipose tissue function was nutritionally regulated.

Methods: Twenty singleton-bearing ewes were either nutrient restricted (NR; consuming 3.2-3.8 megajoules per day of metabolizable energy) or fed to appetite (A; consuming 8.7-9.9 megajoules per day of metabolizable energy) over the period of maximal placental growth, i.e. between 28 and 80 d gestation. After 80 d gestation, ewes were either fed to calculated requirements (R; consuming 6.7-7.5 megajoules per day) or were fed to appetite (A; consuming 8.0-10.9 megajoules per day).

Perirenal adipose tissue was sampled after euthanasia from all ewes at 140 days gestation (n= 5 per group). Total RNA was extracted. The abundance of mRNA species for leptin, UCP1, long and short forms of the prolactin receptor (lPRLR and sPRLR, respectively) were then examined by RT-PCR.

Results: Regardless of dietary challenge lPRLR and sPRLR were tightly correlated (R2 0.88-0.97, P<0.05). Abundance of both leptin and UCP1 mRNA's were strongly correlated with PRLR mRNA's (R2 0.59-0.95, P<0.05) only when mothers were fed to requirements over the second half of gestation.

Conclusion: The PRLR can regulate both brown (i.e. UCP1) and white (i.e. leptin) characteristics of fetal fat, but only when maternal nutrition is restricted in late gestation. The extent to which this effect may be mediated by fetal prolactin has yet to be determined.

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