[Regulation of thermoregulatory thermogenesis]

Two modes of heat production exist which are involved in body temperature regulation with decreasing environmental temperature: shivering thermogenesis and more efficient nonshivering thermogenesis (NST). Enhanced NST is mediated by the activated sympathetic nervous activity and increased secretions of hormonal factors such as glucagon through an enhanced lipid utilization. Moreover, cold acclimation causes an increased responsiveness of the organism to these factors. Noradrenaline-induced secretion of glucagon is also enhanced by cold acclimation. Chronic administration of glucagon simulates cold acclimation, resulting in an improved cold tolerance by an increased NST. Brown adipose tissue (BAT) is a major site for nonshivering thermogenesis (NST) during metabolic cold acclimation. Cold acclimation causes a hyperplasia as well as an enhanced metabolic capacity of BAT cell. BAT function is mainly regulated by sympathetic noradrenaline and several hormonal factors such as glucagon. BAT possesses rich blood supply by which its high thermogenic capacity and an efficient transfer of heat are maintained. Noradrenaline and glucagon increases not only heat production, but also blood flow in BAT. Nitric oxide (NO), endothelium-derived relaxing factor, is involved in noradrenaline-, glucagon- and cold-induced increases of blood flow through BAT. Noradrenaline-induced BAT thermogenesis is suggested to be mediated by NO. NO synthase occurs in BAT cell in addition to endothelium of BAT vessel. These findings indicate that NO may be a signalling molecule for an enhanced NST during cold acclimation. Moreover, BAT contributes to adaptation to overfeeding, nonthermal stress and fever by means of producing heat, playing a role as adaptive organ in overall energy metabolism.