Control of lipolysis by a population of oxytocinergic sympathetic neurons.

Overview

Oxytocin (OXT), a nine-amino-acid peptide produced in the hypothalamus and released by the posterior pituitary, has well-known actions in parturition, lactation and social behaviour¹, and has become an intriguing therapeutic target for conditions such as autism and schizophrenia². Exogenous OXT has also been shown to have effects on body weight, lipid levels and glucose homeostasis^1,3, suggesting that it may also have therapeutic potential for metabolic disease^1,4. It is unclear, however, whether endogenous OXT participates in metabolic homeostasis. Here we show that OXT is a critical regulator of adipose tissue lipolysis in both mice and humans. In addition, OXT serves to facilitate the ability of β-adrenergic agonists to fully promote lipolysis. Most surprisingly, the relevant source of OXT in these metabolic actions is a previously unidentified subpopulation of tyrosine hydroxylase-positive sympathetic neurons. Our data reveal that OXT from the peripheral nervous system is an endogenous regulator of adipose and systemic metabolism.