Apart from thyroid hormones, as the main hormonal regulators of obligatory thermogenesis, and catecholamines, as major hormonal regulators of facultative thermogenesis, production of heat in homeotherms can also be influenced by steroids. Generally, hormones can influence heat production by regulating the activity of various enzymes of oxidative metabolism, by modulating membrane protein carriers and other membrane or nuclear protein factors. Proton carriers in the inner mitochondrial membrane, known as uncoupling proteins, play the key role in heat dissipation to the detriment of the formation of energy-rich phosphates. In this minireview we have focused on the effects of steroids and thyroid hormones on heat production in brown adipose tissues and in skeletal muscles, with particular respect to their effect on uncoupling protein expression. Apart from hormonal steroids, dehydroepiandrosterone, an important precursor in the metabolic pathway leading to hormonal steroids which possess many, mostly beneficial effects on human health, modulates metabolic pathways which may lead to increased heat production. Recent studies demonstrate that 7-oxo-dehydroepiandrosterone, one of its 7-oxygenated metabolites, is even more effective than dehydroepiandrosterone. Recent findings of various actions of these steroids support the view that they may also participate in modulating thermogenic effects.
Interscapular brown adipose tissue (IBAT) activity is controlled by sympathetic nervous system, and factors that influence thermogenesis appear to be centrally connected to the sympathetic outflow to IBAT. Cold exposure produces a rise in BAT temperature, which is associated with an increased thyroid activity, elevated serum levels of 3,5,3’-triiodothyronine (T3), and an increased rate of T3 production. This study evaluated the effect of swimming training on 5’-triiodothyronine deiodinase (5’-D) activity in IBAT under normal environmental conditions and after short (30 min) cold exposure (TST stimulation test). 5’-D activity is lower in trained rats at basal condition, and TST increases 5’-D in IBAT of both untrained and trained rats. However, this increase is lower in trained rats. Training reduces the deiodinating activity in normal environmental conditions as well as after short cold exposure. Probably, other compensatory mechanisms of heat production are active in trained rodents.