Adipose Tissue Development During Early Postnatal Life in Ewe-Reared Lambs

Abstract

SUMMARYThis study examines the precise time course that brown adipose tissue (BAT) takes to adopt the characteristics of white adipose tissue in postnatal lambs. Perirenal adipose tissue was sampled from ewe-reared lambs within 1 h of birth and at 1, 2, 4, 7, 14, 21 and 30 days of age and analysed for the amount of mRNA for uncoupling protein (UCP), the amount and activity of UCP, and protein, mitochondrial protein and lipid content. This was combined with measurements of colonic temperature and jugular venous plasma concentrations of thyroid hormones and insulinlike growth factor-I (IGF-1). Over the first 4-7 days of age, large quantities of UCP mRNA were associated with a peak in plasma triiodothyronine concentration at 2 days of age followed by a maximal amount and activity of UCP at 4 days and a basal colonic temperature of 39 3°C. Between 7 and 30 days there was a large increase in lipid deposition as the amount and activity of UCP and the amount of UCP mRNA declined to basal values and colonic temperature was maintained at 40 'C. A significant positive relationship between perirenal adipose tissue lipid content and plasma IGF-1 concentration was observed throughout the study period. It is concluded that ovine adipose tissue maturation occurs in two distinct phases over the first month of life. The precise time scale of this process could be regulated in part by the lamb's body temperature which determines whether adipose tissue is required for heat production (i.e. BAT) or as an endogenous energy source (i.e. white adipose tissue).

Brown adipose tissue: physiological function and evolutionary significance

“…The disappearance rate of BAT varies between species. In rabbits, BAT disappears about one month after birth (Cambon et al 1998); in bovine and ovine within 2-30 days after birth (Gemmell et al 1972;Casteilla et al 1989;Clarke et al 1997a;Pope et al 2014); and in goats within 2-6 days after birth (Thompson and Jenkinson 1969;Vatnick et al 1987). The signaling pathways atrophying BAT are not fully understood.…”

Adipose tissue and fetal programming

“…In rodents, the primary BAT depot is interscapular, retains UCP1 throughout the life cycle and is located within a layer of white adipose tissue. In contrast, in both large mammals and humans, the major source of BAT in the fetus is around the central organs, a depot that is replaced by white fat after birth [15]. The main BAT depot in adult humans is in the supraclavicular region which weighs ∼40-50 g [7,16,17].…”

“…Moreover, as discussed in more detail below, the ability of the placenta to adapt to any nutritional intervention, and thus minimise changes in nutrient supply to the fetus, will be dependent on the timing of the maternal challenge [32]. Maximal [79] Decreases with age [15] Nutritional interventions during pregnancy and their impact on fetal adipose tissue…”

“…Consequently, targeted changes of the in utero nutritional environment could contribute to early perturbations in glucose/insulin signalling, as observed in the metabolic syndrome, even in the absence of any absolute changes in adipose tissue mass, at least in sheep [48]. One reason for this is that, in sheep, fat growth in is most rapid through lactation [15], when both maternal body weight [49] and parity [50] can have a much greater effect than changes in maternal diet. This could further explain why only very modest effects can be seen in the offspring during young adulthood compared with those seen in response to exposure to an obesogenic environment.…”

Heifer nutrient intake during early- and mid-gestation programs adult offspring adiposity and mRNA expression of growth-related genes in adipose depots

“…The PR depot is the largest depot of brown adipose tissue in the newborn calf and plays a fundamental role in neonatal thermogenesis and survival prior to its transition to a white adipose storage depot by the end of the first month of life (Clarke et al 1997). The successful conversion of preadipocytes to mature lipidcontaining adipocytes requires IGF1 (Smith et al 1988, Gregoire et al 1998.…”