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1 Centre for Reproduction and Early Life, Institute of Clinical Research, University of Nottingham, Nottingham, United Kingdom
* To whom correspondence should be addressed. E-mail: michael.symonds{at}nottingham.ac.uk.
Increased glucocorticoid action and adipose tissue inflammation contribute to excess adiposity. These adaptations may be enhanced in offspring exposed to nutrient restriction (NR) in utero thereby increasing their susceptibility to later obesity. We therefore determined the developmental ontogeny of glucocorticoid receptor (GR), 11
-hydroxysteroid dehydrogenase (11HSD) type 1 and 2 and uncoupling protein (UCP)-2 mRNA in perirenal adipose tissue between late gestation and 6 months after birth in the sheep, as well as the effect of maternal NR targeted between early to mid (28-80 days, term ~147 days) or late (110-147 days) gestation. GR and 11HSD1 mRNA increased with fat mass and were all maximal within the 6 month observation period. 11HSD2 mRNA abundance demonstrated a converse decline whilst UCP2 peaked at 30 days. GR and 11HSD1 mRNA abundance were strongly correlated with total and relative perirenal adipose tissue weight, and UCP2 with GR and 11HSD1 mRNA. Early to mid gestational NR increased GR, 11HSD1 and UCP2 mRNA, but decreased 11HSD2 mRNA abundance; an adaptation reversed with late gestational NR. We conclude that the continual rise in glucocorticoid action and fat mass after birth may underlie the development of later obesity. The magnitude of this adaptation is partly dependent on maternal food intake through pregnancy.
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