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Increased thyroid hormone concentrations lead to heat production via general stimulation of metabolism (obligatory thermogenesis) and possibly via activation of thyroid hormone receptors and uncoupling protein 1 (UCP 1) and deiodinase enzyme genes in the brown adipose tissue (BAT). In human subjects long\u2010term cold exposures do not seem to activate the pituitary\u2010thyroid axis, but rather accelerate the elimination of triiodothyronine (T3), leading to low serum concentrations of free T3 hormone. In corollary to this a hypothyreotic condition with increased serum thyroid\u2010stimulating hormone and impaired mood and cognitive performance can be observed after long\u2010term cold exposures such as wintering. During cold exposures the sympathetic nerve system is activated and noradrenaline is released to blood circulation and to BAT, where it leads to production of cAMP, lipolysis and free fatty acids. Free fatty acids open the mitochondrial proton channel protein in BAT. Protons enter the mitochondria and inhibit ATP synthesis (uncoupling). By this way energy is transformed into heat (facultatory or adaptive thermogenesis). In adult human subjects the amount of BAT is small and adaptive thermogenesis (non\u2010shivering thermogenesis) has a smaller role. UCP 1 with other uncoupling proteins may have other functions in the control of body weight, sugar balance and formation of reactive oxygen species.<\/jats:p>","DOI":"10.1111\/j.1365-201x.2005.01464.x","type":"journal-article","created":{"date-parts":[[2005,7,15]],"date-time":"2005-07-15T13:50:38Z","timestamp":1121435438000},"page":"255-264","source":"Crossref","is-referenced-by-count":65,"title":["Pituitary and autonomic responses to cold exposures in 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