Postnatal selective suppression of lipoprotein lipase gene expression in brown adipose tissue (relative to the expression of the gene for the uncoupling protein) is not due to adrenergic insensitivity: a possible specific inhibitory effect of colostrum

Abstract

The levels of mRNA coding for the uncoupling protein (UCP) and for lipoprotein lipase (LPL) were monitored in the brown adipose tissue of newborn rat pups. At 5 h after birth, the mRNA levels of UCP and LPL were high in pups exposed singly to 28 degrees C and low in pups kept singly at thermoneutrality (36 degrees C); in pups staying with the dam, the UCP mRNA levels were intermediate. However, the LPL mRNA levels were lower in pups staying with the dam than in pups at 36 degrees C, implying that factors additional to environmental temperature influenced LPL gene expression. Injection of noradrenaline into pups at thermoneutrality (36 degrees C) led to increases in UCP and LPL gene expression, but noradrenaline injections had no further effect in cold-exposed pups. The adrenergic effects were mediated via beta-adrenergic receptors. The cold-induced increases in both UCP and LPL gene expression were abolished by the beta-adrenergic antagonist propranolol. Thus differences in adrenergic responsiveness could not explain the differential expression of the UCP and LPL genes observed in pups staying with the dam. The presence of a physiological suppressor was examined by feeding single pups at 28 degrees C with different foods: nothing, water, Intralipid, cow's milk, rat milk and rat colostrum. None of these agents led to suppression of UCP gene expression, but colostrum led to a selective suppression of LPL gene expression. It was concluded that the genes for UCP and LPL were responsive to adrenergic stimuli immediately after birth, and it is suggested that a component of rat colostrum can selectively suppress LPL gene expression.

Integration of physiological and molecular mechanisms of the developmental origins of adult disease: new concepts and insights

“…In the latter species brown adipose tissue is rapidly activated at birth, as both sheep and human subjects are precocial thermoregulators (Clarke et al 1997b). For altricial thermoregulators, such as the rat, their brown fat is not fully activated until they start to leave their nest, which is coincident with maturation of their hypothalamic-pituitary axis (Obregon et al 1996). Furthermore, in sheep, but not rats, perirenal adipose tissue is the most-rapidly-growing tissue after birth (Clarke et al 1997a), although the extent to which this process can be preferentially promoted has yet to be shown.…”

The effect of maternal prolactin infusion during pregnancy on fetal adipose tissue development

“…Fetal adipose tissue maturation is characterised by the appearance of the brown adipose tissue-specific uncoupling protein-1 (UCP1), which occurs over the final half of gestation in the ovine fetus (Clarke et al 1997b). In rat pups, however, the potential thermogenic activity and UCP1 content primarily increase over the first few days of postnatal life (Obregon et al 1996), reaching a maximum at around day 5 (Sundin & Cannon 1980). Maturation of fetal adipose tissue is not confined to changes in UCP1 but may include voltage-dependent anion channel (VDAC) which is an outer mitochondrial membrane protein.…”

Melanocortinergic Activation by Melanotan II Inhibits Feeding and Increases Uncoupling Protein 1 Messenger Ribonucleic Acid in the Developing Rat

“…However, under certain conditions, such as low ambient temperature, BAT thermogenesis may be critical for survival through defense of body temperature. Indeed, as early as 5 h after birth, rodent neonates can increase UCP1 levels in response to either cold or ␤-adrenergic stimulation (28). Our findings suggest that sympathetic outflow to BAT, mediated through melanocortin receptor acti- vation, is functional and responsive at birth.…”