Thermogenesis and the energetics of pregnancy and lactation.
Energy balance studies suggest that the overall efficiency of energy utilization does not increase during pregnancy in rodents, other than as a consequence of "hyperphagia". Diet-induced thermogenesis is not stimulated in response to the increased energy intake of the pregnant animal, the extra intake being retained at the maximum efficiency. Biochemical studies on brown adipose tissue, the main site of adaptive thermogenesis in rodents, are consistent with the energy balance data, at least in rats and mice. However, in hamsters (golden and Djungarian) some atrophy of the tissue is evident during pregnancy. In contrast to pregnancy, the thermogenic activity (mitochondrial GDP binding) and capacity (uncoupling protein content) of brown adipose tissue are substantially reduced during lactation in rats and mice. These changes result from a fall in sympathetic activity in the tissue in lactation. Sympathetic activity and thermogenic capacity are, however, fully restored following weaning of the pups. The functional atrophy of brown adipose tissue during lactation is linked to a substantial saving in maternal energy expenditure, reducing the energy requirements for milk production. The lactating-post-lactating animal provides an excellent example of a physiologically programmed reversible atrophy of brown adipose tissue.[1]References
- Thermogenesis and the energetics of pregnancy and lactation. Trayhurn, P. Can. J. Physiol. Pharmacol. (1989) [Pubmed]
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