Exploring a new mechanism controlling thermogenesis of adipose tissue

Adipose tissue dissipates energy for thermogenesis, a heat-generating process that helps maintain body temperature. Sympathetic nerves release norepinephrine (NE) to increase thermogenesis of adipose tissue during cold stimulation. However, other factors that regulate adipose tissue thermogenesis should not be ignored. We hypothesized that some neuroactive factors also participate in regulating adipose tissue thermogenesis. We exposed mice to ambient temperatures of 4°C, 22°C, and 30°C and found that the thermogenesis of inguinal white adipose tissue (iWAT) increased after moving from 22°C to 4°C for 3 days, and decreased after moving from 22°C to 30°C for 3 days. We observed that iWAT is mainly innervated by three nerve bundles and verified that these nerves contained adrenergic nerves but no cholinergic nerves. While NE levels increased at 4°C as expected, they did not decrease at 30°C, which does not correlate with the decrease in thermogenesis observed. Further analysis revealed the expression of multiple receptors for hypothalamus/pituitary neuroendocrine hormones in adipocytes. Among these pituitary hormones, arginine vasopressin (AVP) decreased the expression of uncoupling protein 1 (UCP1) for thermogenesis, whereas oxytocin (OXT) increased UCP1 expression. Our results suggested that in addition to the sympathetic nerves, some neuroendocrine hormones regulate adipose tissue thermogenesis. Therefore, the observed changes in thermogenesis may be a result of synergic regulation of neurotransmitters and neuroendocrine hormones.