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  • Title: Differential effects of fetal number and maternal nutrition in late gestation on prolactin receptor abundance and adipose tissue development in the neonatal lamb.
    Author: Budge H, Dandrea J, Mostyn A, Evens Y, Watkins R, Sullivan C, Ingleton P, Stephenson T, Symonds ME.
    Journal: Pediatr Res; 2003 Feb; 53(2):302-8. PubMed ID: 12538790.
    Abstract:
    The present study examined the extent to which abundance of the prolactin receptor (PRLR) and a range of primary mitochondrial proteins are influenced by either maternal nutrition and/or fetal number in adipose tissue. Pregnant sheep were control fed [consuming 100% of total metabolizable energy (ME) requirements (taking into account requirements for both ewe maintenance and growth of the conceptus to produce a 4.5-kg lamb at term) for that stage of gestation] or were nutrient restricted (consuming 60% of total ME requirements). All ewes lambed normally at term and both perirenal adipose and hepatic tissues were sampled within 6 h of birth. Plasma membranes and mitochondria were prepared and analyzed using immunoblotting for abundance of PRLR and/or cytochrome c, voltage-dependent anion channel (VDAC), and uncoupling protein-1 (UCP1). Irrespective of maternal nutrition, abundance of specific isoforms of PRLR were significantly higher in adipose tissue sampled from twins compared with singletons and total UCP1 concentration per milligram of tissue was increased (p < 0.05). There was no effect of fetal number on PRLR abundance in the liver. Maternal nutrient restriction resulted in an increased abundance of both cytochrome c (p < 0.001) and VDAC in adipose tissue of twins but not singletons. This occurred despite maternal nutrition having no effect on either lamb body or adipose tissue weights, although both were lower (p < 0.05) in twins compared with singletons. In conclusion, fetal adipose tissue development is highly sensitive to nutritionally mediated changes in late gestation. An increase in fetal number results in greater PRLR abundance, which, in conjunction with a decrease in maternal nutrition, results in up-regulation of specific mitochondrial proteins.
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