Non-shivering thermogenesis in brown adipose tissue (BAT) of precocial newborns, such as sheep, is essential for effective adaptation to cold exposure of the extra-uterine environment. A suboptimal nutritional environment in utero can reprogramme adipose tissue development and function[1] and, is associated with excess adiposity in later life although the precise mechanism(s) by which this occurs are not fully established. Maternal nutrient restriction in late gestation, coincident with appearance of large amounts of the BAT specific uncoupling protein (UCP)1, restricts its synthesis [2]. The aim of the present study was, therefore, to examine the extent to which factors associated with enhancing, or suppressing, UCP1 gene expression maybe reset in newborn sheep born to nutrient restricted (NR) mothers. Methods: Twin bearing Border Leicester cross Swaledale sheep of similar age and body fat distribution were individually housed at 110 days of gestation and randomly assigned to receive either 100% of metaboliseable energy (ME) requirements for body weight and stage of gestation (i.e. controls; n=8) or 60% of this amount (i.e. NR; n=9). Then, within 12 hours of birth, one twin from each mother was randomly selected and humanely euthanased with an intra-venous injection of barbiturate for tissue sampling. All procedures were conducted with Home Office Approval under UK legislation. Gene expression for regulators of UCP1 synthesis was determined using qPCR. Their expression was calculated using the ΔΔCt method and expressed relative to the geometric mean of 3 reference genes (IPO8, RSP2 and YWAZ), normalised to the control group and expressed in arbitrary units. Data are presented as mean ± SE and were compared between groups using a Mann-Whitney test. Results: In accord with previous findings[2], there was a trend towards a reduction in UCP1 gene expression in offspring born to NR mothers (C: 1 ± 0.19; NR: 0.6 ± 0.12 (p=0.07)) this was accompanied by reduced mRNA abundance for type II iodothyronine deiodinase (DIO2) (C: 1 ± 0.23; NR: 0.44 ± 0.10 (p <0.05)). In contrast, the expression of RIP140 was increased (C: 1 ± 0.14; NR: 1.77± 0.20 (p<0.05)) as was that of PPARΥ (C: 1± 0.10; NR: 1.60 ± 0.17). The expression of other genes associated with adipogenesis such as Cidea and TWIST I was unchanged. Conclusion: Reduced UCP1 abundance following maternal nutrient restriction coincident with the time of its rapid appearance results in a complex set of adaptations linked to multiple pathways controlling UCP1 transcription. As UCP1 is lost through postnatal life, these would be predicted to subsequently promote white adipose tissue deposition and thus may contribute to excess adiposity in later life.