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This version published online on June 16, 2005
Endocrinology, doi:10.1210/en.2005-0246
A more recent version of this article appeared on September 1, 2005
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Medline Plus Health Information
*High Risk Pregnancy
*Nutrition

Submitted on March 1, 2005
Accepted on June 3, 2005

Maternal nutritional programming of fetal adipose tissue development: differential effects on mRNA abundance for uncoupling proteins, peroxisome proliferator activated and prolactin receptors

J. Bispham, D. S. Gardner, M. G. Gnanalingham, T. Stephenson, M. E. Symonds*, and H. Budge

Centre for Reproduction and Early Life, Institute of Clinical Research, University of Nottingham NG7 2UH, U.K.

* To whom correspondence should be addressed. E-mail: michael.symonds{at}nottingham.ac.uk.

Maternal nutrient restriction at specific stages of gestation has differential effects on fetal development such that the offspring are programed to be at increased risk of a range of adult diseases including obesity. We investigated the effect of maternal nutritional manipulation through gestation on fetal adipose tissue deposition in conjunction with mRNA abundance for uncoupling protein (UCP)1 and 2, peroxisome proliferator activated receptors (PPAR) {alpha} and {gamma}, together with long and short forms of the prolactin receptor (PRLR). Singleton bearing ewes were either nutrient restricted (NR; 3.2-3.8 MJ day-1 metabolisable energy) or fed to appetite (8.7-9.9 MJ day-1) over the period of maximal placental growth i.e. between 28 to 80 days gestation. After 80 days gestation, ewes were either fed to calculated requirements, (6.7-7.5 MJ day-1), or to appetite (8.0-10.9 MJ day-1). At term, offspring of NR ewes possessed more adipose tissue, an adaptation that was greatest in those born to mothers that fed to requirements in late gestation. This was accompanied by an increased mRNA abundance for UCP2 and PPAR {alpha}, an adaptation not seen in mothers re-fed to appetite. Maternal nutrition had no effect on mRNA abundance for UCP1, PPAR {gamma} or PRLR. Irrespective of maternal nutrition, mRNA abundance for UCP1 was positively correlated with PPAR {gamma} and the long and short forms of PRLR indicating that these factors may act together to ensure UCP1 abundance is maximized in the newborn. In conclusion, we have shown, for the first time, differential effects of maternal nutrition on key regulatory components of fetal fat metabolism.
Key words: Nutrition • Uncoupling proteins • Prolactin receptors




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