Introduction: Leptin, the product of the obese (ob) gene is secreted predominantly, but not exclusively, from adipose tissue. Fetal plasma concentrations of leptin increase with gestational age in conjunction with an increase in fetal adipose tissue deposition and mRNA abundance for leptin and UCP-1. The present study aimed to determine the effect of chronic fetal leptin infusion on UCP-1 and voltage dependent anion channel (VDAC; located on the outer mitochondrial membrane) abundance.
Methods: Perirenal adipose tissue was sampled after euthanasia from near-term fetuses (141 days gestation), infused with ovine leptin (1.0-1.5 mg/kg/d; n=6) or saline alone (n=5) from 137 days gestation . Mitochondria were prepared and abundance of UCP-1 and VDAC determined by immunoblotting.
Results (mean ± s.e.m) are presented as % of a reference sample (1 day old lamb). Results: Leptin infusion resulted in higher UCP-1 abundance (Leptin 74±9; Saline 53±1 % ref (P=0.07)) but no change in adipose tissue weight or VDAC abundance (Leptin 128±13; Saline 148±15 % ref).
Conclusion: Leptin promotes the appearance of UCP-1 during late gestation in preparation for the rapid increase in heat production after birth. It remains to be determined whether this is a direct effect or mediated by changes in activity of the sympathetic nervous system or thyroid hormone secretion.
Y Evens was funded by a Wellcome Trust Vacation Scholarship and S Pearce was supported by a BBSRC Postgraduate Studentship.
03 - 04 Dec 2001
Society for Endocrinology