It is now established that the role and/or abundance of both UCP1 and 2 changes dramatically over the perinatal period and that the magnitude of this adaptation is dependent on maturity at birth. In sheep, for example,the brown adipose tissue specific UCP1 is lost soon after birth, whilst a similar transition is seen for UCP2 in the lung. In contrast, gene expression for UCP2 in adipose tissue peaks during the postnatal period coincident with the large increase in white adipose tissue deposition. The magnitude of these adaptations is substantially influenced by the prenatal environment and as such can be reprogrammed by changes in maternal dietary intake. Critically these responses persist into later life when they may not necessarily accompany increases in fat mass. At the same time UCP2 gene expression can be enhanced in a tissue specific manner that is dependent on the stage of embryonic or fetal development in which the mother is nutritionally manipulated. These adaptations are mediated in part by changes in tissue glucocorticoid action which similarly vary between tissues and stage of development. The talk will thus summarise our recent findings on the impact of prenatal maternal nutrient restriction and its long term influence on UCP abundance in individuals that are habituated to either a sedentary or active life style.