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Brown Adipose Tissue Thermogenesis During Aging and Senescence
Authors:Roger B McDonald  Barbara A Horwitz
Institution:(1) Department of Nutrition Division of Biological Sciences, University of California, Davis, California, 95616-8669;(2) Section of Neurobiology, Physiology, and Behavior, Division of Biological Sciences, University of California, Davis, California, 95616-8669
Abstract:We have found that cold- and norepinephrine-induced brown adipose tissue (BAT) nonshiveringthermogenesis (NST) is significantly lower in old male Fischer 344 rats and is associatedwith the decreased ability of these animals to maintain homeothermy. This decline in BATthermogenesis is not as great in females. Although the mechanism(s) underlying this genderdifference in the age-related decrease in brown fat NST are not completely elucidated, theydo not appear to reflect decreased sympathetic neural activity of BAT in the older males vs.females. Rather, our investigations, strongly suggest that the blunted cold-induced heatproduction of BAT reflects less functional BAT. The fact that the older animals have less functionalBAT than do their younger counterparts may predispose them to the accumulation of excessbody fat. Our studies have also found that near the end of the natural life of these rats, theyenter a state of senescence that can be identified by spontaneous rapid body weight loss,resulting from decreased food intake. In this state, the rats are considerably more susceptibleto cold than are comparably aged presenescent (body weight stable) rats of the samechronological age. The greater hypothermia exhibited by the senescent vs. presenescent rats during coldexposure is associated with a significant reduction in the amount of functional brown fat andin the amount of heat each brown fat cell can generate. It is the intent of this review to discussthe findings of these investigations.
Keywords:Brown adipocyte proliferation  cold exposure  nonshivering thermogenesis  norepinephrine  sympathetic nervous system  uncoupling protein one (UCP1)
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