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1 Centre for Reproduction and Early Life, Institute of Clinical Research, University of Nottingham NG7 2UH, UK
2 Department of Physiology, University of Cambridge, Downing Street, Cambridge CB2 3EG, UK
The endocrine regulation of uncoupling protein-2 (UCP2), an inner mitochondrial protein, in fetal adipose tissue remains unclear. The present study aimed to determine if fetal plasma cortisol and triiodothyronine (T3) influenced the mRNA abundance of UCP2, glucocorticoid receptor (GR) and 11ß-hydroxysteroid dehydrogenase type 1 (11ßHSD1) and 2 (11ßHSD2) in fetal adipose tissue in the sheep during late gestation. Perirenal–abdominal adipose tissue was sampled from ovine fetuses to which either cortisol (2–3 mg kg–1 day–1) or saline was infused for 5 days up to 127–130 days gestation, or near term fetuses (i.e. 142–145 days gestation) that were either adrenalectomised (AX) or remained intact. Fetal plasma cortisol and T3 concentrations were higher in the cortisol infused animals and lower in AX fetuses compared with their corresponding control group, and increased with gestational age. UCP2 and GR mRNA abundance were significantly lower in AX fetuses compared with age-matched controls, and increased with gestational age and by cortisol infusion. Glucocorticoid action in fetal adipose tissue was augmented by AX and suppressed by cortisol infusion, the latter also preventing the gestational increase in 11ßHSD1 mRNA and decrease in 11ßHSD2 mRNA. When all treatment groups were combined, both fetal plasma cortisol and T3 concentrations were positively correlated with UCP2, GR and 11ßHSD2 mRNA abundance, but negatively correlated with 11ßHSD1 mRNA abundance. In conclusion, plasma cortisol and T3 are both required for the late gestation rise in UCP2 mRNA and differentially regulate glucocorticoid action in fetal adipose tissue in the sheep during late gestation.
(Received 24 May 2005;
accepted after revision 9 June 2005;
first published online 16 June 2005)
Corresponding author M. E. Symonds: Academic Division of Child Health, School of Human Development, Queen's Medical Centre, University Hospital, Nottingham NG7 2UH, UK. Email: michael.symonds{at}nottingham.ac.uk
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