Document Type

Article

Publication Date

12-9-2020

Keywords

JMG

JAX Source

Mol Med 2020 Dec 9; 26(1):126

Volume

26

Issue

1

First Page

126

Last Page

126

ISSN

1528-3658

PMID

33297933

DOI

https://doi.org/10.1186/s10020-020-00254-3

Abstract

BACKGROUND: Innervation of adipose tissue is essential for the proper function of this critical metabolic organ. Numerous surgical and chemical denervation studies have demonstrated how maintenance of brain-adipose communication through both sympathetic efferent and sensory afferent nerves helps regulate adipocyte size, cell number, lipolysis, and 'browning' of white adipose tissue. Neurotrophic factors are growth factors that promote neuron survival, regeneration, and plasticity, including neurite outgrowth and synapse formation. Peripheral immune cells have been shown to be a source of neurotrophic factors in humans and mice. Although a number of immune cells reside in the adipose stromal vascular fraction (SVF), it has remained unclear what roles they play in adipose innervation. We previously demonstrated that adipose SVF secretes brain derived neurotrophic factor (BDNF).

METHODS: We now show that deletion of this neurotrophic factor from the myeloid lineage of immune cells led to a 'genetic denervation' of inguinal subcutaneous white adipose tissue (scWAT), thereby causing decreased energy expenditure, increased adipose mass, and a blunted UCP1 response to cold stimulation.

RESULTS: We and others have previously shown that noradrenergic stimulation via cold exposure increases adipose innervation in the inguinal depot. Here we have identified a subset of myeloid cells that home to scWAT upon cold exposure and are Ly6C

CONCLUSIONS: We propose that these myeloid lineage, cold induced neuroimmune cells (CINCs) are key players in maintaining adipose innervation as well as promoting adipose nerve remodeling under noradrenergic stimulation, such as cold exposure.

Comments

This article is licensed under a Creative Commons Attribution 4.0 International License.

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