Journal
PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY
Volume 470, Issue 5, Pages 823-837Publisher
SPRINGER
DOI: 10.1007/s00424-017-2090-z
Keywords
Brown adipose tissue; Feeding; Hunger; Metabolism; Sympathetic; Thermoregulation
Categories
Funding
- Funding Program for Next GenerationWorld-Leading Researchers from the Japan Society for the Promotion of Science [LS070]
- Ministry of Education, Culture, Sports, Science and Technology of Japan [17K08568, 23790271, 26860159, 16H05128, 15H05932, 15K21744, 26118508, 26713009]
- PRESTO program of the Japan Science and Technology Agency [JPMJPR13M9]
- Project for Elucidating and Controlling Mechanisms of Aging and Longevity from the Japan Agency for Medical Research and Development
- Hori Science and Arts Foundation
- Takeda Science Foundation
- Nakajima Foundation
- Uehara Memorial Foundation
- Brain Science Foundation
- Kowa Life Science Foundation
- Grants-in-Aid for Scientific Research [26118508, 26713009, 16H05128, 15K21744, 26860159, 17K08568, 15H05932, 23790271] Funding Source: KAKEN
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Energy homeostasis of mammals is maintained by balancing energy expenditure within the body and energy intake through feeding. Several lines of evidence indicate that brown adipose tissue (BAT), a sympathetically activated thermogenic organ, turns excess energy into heat to maintain the energy balance in rodents and humans, in addition to its thermoregulatory role for the defense of body core temperature in cold environments. Elucidating the central circuit mechanism controlling BAT thermogenesis dependent on nutritional conditions and food availability in relation to energy homeostasis is essential to understand the etiology of symptoms caused by energy imbalance, such as obesity. The central thermogenic command outflow to BAT descends through an excitatory neural pathway mediated by hypothalamic, medullary and spinal sites. This sympathoexcitatory thermogenic drive is controlled by tonic GABAergic inhibitory signaling from the thermoregulatory center in the preoptic area, whose tone is altered by body core and cutaneous thermosensory inputs. This circuit controlling BAT thermogenesis for cold defense also functions for the development of fever and psychological stress-induced hyperthermia, indicating its important role in the defense from a variety of environmental stressors. When food is unavailable, hunger-driven neural signaling from the hypothalamus activates GABAergic neurons in the medullary reticular formation, which then block the sympathoexcitatory thermogenic outflow to BAT to reduce energy expenditure and simultaneously command the masticatory motor system to promote food intake-effectively commanding responses to survive starvation. This article reviews the central mechanism controlling BAT thermogenesis in relation to the regulation of energy and thermal homeostasis dependent on food availability.
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