Sensory denervation of inguinal white fat modifies sympathetic outflow to white and brown fat in Siberian hamsters.

White adipose tissue (WAT) and brown adipose tissue (BAT) have sympathetic nervous system (SNS) and sensory innervations. Previous studies from our laboratory revealed central neuroanatomical evidence of WAT sensory and BAT SNS crosstalk with double labeling of inguinal WAT (IWAT) sensory and interscapular BAT (IBAT) SNS neurons. We previously demonstrated that WAT lipolysis increases IBAT temperature, but this effect is absent when IWAT afferents are surgically denervated, which severs both sensory and SNS nerves. It is possible that WAT sensory feedback can regulate SNS drive to itself and other WAT and BAT depots, and thus contribute to the existence of differential SNS outflow to fat during different energy challenges. Here we selectively denervated IWAT sensory nerves in Siberian hamsters using capsaicin and measured norepinephrine turnover (NETO) i.e., SNS drive to WAT and BAT depots, IBAT uncoupling protein 1 (UCP1) expression, body mass, fat mass, blood glucose, and food consumed after a 24-h cold exposure. IWAT sensory denervation decreased both IWAT and IBAT NETO and IBAT UCP1 expression. IWAT sensory denervation, however, increased mesenteric WAT (MWAT) NETO after the 24-h cold exposure and did not modify epididymal WAT (EWAT) and retroperitoneal WAT (RWAT) NETO compared with respective controls. Body mass, fat mass, blood glucose, and food consumed were unchanged across groups. RWAT and EWAT mass decreased in capsaicin-injected hamsters, but did not in the vehicle hamsters. These results functionally demonstrate the existence of IWAT sensory and IBAT SNS crosstalk and that a disruption in this sensory-SNS feedback mechanism modifies SNS drive to IWAT, IBAT, and MWAT, but not EWAT and RWAT.