Control of lipolysis by a population of oxytocinergic sympathetic neurons

Erwei Li, Luhong Wang, Daqing Wang, Jingyi Chi, Zeran Lin, Gordon I. Smith, Samuel Klein, Paul Cohen and Evan D. Rosen ()
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Erwei Li: Beth Israel Deaconess Medical Center
Luhong Wang: Beth Israel Deaconess Medical Center
Daqing Wang: Beth Israel Deaconess Medical Center
Jingyi Chi: Harvard Medical School
Zeran Lin: The Rockefeller University
Gordon I. Smith: Washington University School of Medicine
Samuel Klein: Washington University School of Medicine
Paul Cohen: The Rockefeller University
Evan D. Rosen: Beth Israel Deaconess Medical Center

Nature, 2024, vol. 625, issue 7993, 175-180

Abstract: Abstract 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 homeostasis1,3, suggesting that it may also have therapeutic potential for metabolic disease1,4. 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.

Date: 2024
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DOI: 10.1038/s41586-023-06830-x

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