Older rats exposed to low environmental temperature show attenuated thermogenesis. However, the mechanisms responsible for this attenuation are not clear. This investigation evaluated the possibility that reduced nonshivering thermogenic capacity is associated with this attenuation. O2 consumption was measured in male Fischer 344 rats ages 7 and 24 mo at thermoneutrality (26°C), during exposure to cold (6°C) for 2 h, and during norepinephrine (NE) infusion (an in vivo measure of nonshivering thermogenesis). In addition, the binding of GDP to isolated mitochondria of brown fat, an in vitro estimate of nonshivering thermogenesis, was also measured. Resting mass-independent O2 consumption (ml·min-1·g body mass-0.67) was not different between the two age groups. However, mass-independent O2 consumption was significantly greater in the younger vs. older rats during 2 h of cold exposure (younger, 2.86 ± 0.19 l/kg body mass0.67; older, 2.39 ± 0.10 l/kg body mass0.67) and during 20 min of maximum NE infusion (younger, 410.4 ± 15.1 ml/kg body mass0.6A7; older, 323.2 ± 31.6 ml/kg body mass0.67). Brown fat mass [absolute (g) as well as relative (g tissue/kg body mass)] was greater in younger than in older rats. Furthermore, younger rats had significantly greater binding of GDP to isolated mitochondria of brown fat than did the older rats. This effect was true whether the data were expressed as nanomoles bound per milligram mitochondrial protein (32% lower in older rats), bound nanomoles recovered (57% lower), or bound picogram per kilogram body mass0.67 (59% lower). The results of this study provide evidence that the age-related loss in cold tolerance of the Fischer 344 rat is, in part, due to a loss in sympathetic-mediated nonshivering thermogenesis.
|Original language||English (US)|
|Journal||American Journal of Physiology - Regulatory Integrative and Comparative Physiology|
|State||Published - 1988|
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