The recognition of significant depots of BAT in adult humans, the inverse correlation
between active BAT and obesity, and the ability of white adipose to be “converted”
to a more “brown-like” phenotype have reinvigorated research in this area. The lack
of active BAT in obesity has been interpreted to suggest that obese adults lack significant
depots of BAT. This seemingly contradicts the observation in rodent models of diet-induced
obesity that BAT (UCP-1 expression) is upregulated. The current studies sought to
resolve this contradiction by testing the hypotheses that BAT is upregulated in diet-induced
obesity but that the sympathetic drive of this tissue is impaired in animals maintained
on a high fat diet. Rats made obese by maintenance on a high fat diet failed to increase
BAT sympathetic nerve activity in response to cooling. In contrast, mRNA for UCP-1
was up regulated by a high fat diet and activation of the sympathetic premotor neurons
in the raphe pallidus with bicuculline resulted in exaggerated increases in BAT SNA
and thermogenesis in rats maintained on a high fat diet compared to those on control
diet. Furthermore, preliminary data suggest that vagal afferent activity and glutamatergic
activation of neurons in the NTS is required for the high fat diet induced inhibition
of BAT SNA and thermogenesis. These data suggest that plasticity in vagal afferent
activity during maintenance on a high fat diet may contribute to weight gain by impairing
metabolism in adipose tissue. Supported by American Diabetes Association Basic Science
grant #1-13-BS-120.
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© 2015 Published by Elsevier Inc.