Abstract
Brown and white adipose tissues are essential for maintenance of proper energy balance and metabolic health. In order to function efficiently, these tissues require both endocrine and neural communication with the brain. Brown adipose tissue (BAT), as well as the inducible brown adipocytes that appear in white adipose tissue (WAT) after simulation, are thermogenic and energy expending. This uncoupling protein 1 (UCP1)-mediated process requires input from sympathetic nerves releasing norepinephrine. In addition to sympathetic noradrenergic signaling, adipose tissue contains sensory nerves that may be important for relaying fuel status to the brain. Chemical and surgical denervation studies of both WAT and BAT have clearly demonstrated the role of peripheral nerves in browning, thermogenesis, lipolysis, and adipogenesis. However, much is still unknown about which subtypes of nerves are present in BAT versus WAT, what nerve products are released from adipose nerves and how they act to mediate metabolic homeostasis, as well as which cell types in adipose are receiving synaptic input. Recent advances in whole-depot imaging and quantification of adipose nerve fibers, as well as other new research findings, have reinvigorated this field of research. This review summarizes the history of research into adipose innervation and brain–adipose communication, and also covers landmark and recent research on this topic to outline what we currently know and do not know about adipose tissue nerve supply and communication with the brain.
Highlights
The brain, and the hypothalamus, is responsible for coordinating energy balance by integrating signals coming from the periphery
Adipose tissue innervation has been studied since the 1890s, and seminal studies were contributed by several research groups in the last few decades
Instead there could be stimulation of vasodilation to tissues due to vasoregulatory innervation and no resulting change in the absolute catecholamine levels delivered to the tissue per volume of blood, but rather an increased volume of blood that would thereby deliver more catecholamines. This idea could provide a vascular mechanism for how obese adipose tissues loses thermogenic capacity, given the vasculature damage that occurs due to chronic inflammation and the relative loss of vascular supply to adipocytes, due to expanding adipose mass coupled with a lack of new angiogenesis, as reviewed by Stapleton et al [11]
Summary
The brain, and the hypothalamus, is responsible for coordinating energy balance by integrating signals coming from the periphery These signals include important endocrine hormones and nutrients from the circulatory system, and feedback from sensory nerves in peripheral tissues and organs. The brain can communicate outwardly to these tissues and organs through distinct efferent peripheral nerves, such as sympathetic nerves For adipose tissue, this incoming sympathetic drive and resulting release of the neurotransmitter norepinephrine (NE) is critical for metabolic processes including lipolysis, adipogenesis, and browning. Several research groups (including ours) have reinvigorated the study of how neural innervation of adipose tissue is regulated, and many new discoveries and advancements in tissue imaging have been made. In this review we summarize historic, landmark, and recent studies that provide insights into the roles of adipose tissue nerves in metabolic function
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