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Brain–adipose tissue cross talk

Published online by Cambridge University Press:  07 March 2007

Timothy J. Bartness*
Affiliation:
Department of Biology, Neurobiology & Behavior Program Center for Behavioral Neuroscience, Georgia State University, Atlanta, GA 30302–4010, USA
C. Kay Song
Affiliation:
Department of Biology, Neurobiology & Behavior Program Center for Behavioral Neuroscience, Georgia State University, Atlanta, GA 30302–4010, USA
Haifei Shi
Affiliation:
Department of Biology, Neurobiology & Behavior Program Center for Behavioral Neuroscience, Georgia State University, Atlanta, GA 30302–4010, USA
Robert R. Bowers
Affiliation:
Department of Biology, Neurobiology & Behavior Program Center for Behavioral Neuroscience, Georgia State University, Atlanta, GA 30302–4010, USA
Michelle T. Foster
Affiliation:
Department of Biology, Neurobiology & Behavior Program Center for Behavioral Neuroscience, Georgia State University, Atlanta, GA 30302–4010, USA
*
* Corresponding author: Dr Timothy J. Bartness, fax +1 404 651 2509, email [email protected]
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Abstract

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While investigating the reversible seasonal obesity of Siberian hamsters, direct sympathetic nervous system (SNS) postganglionic innervation of white adipose tissue (WAT) has been demonstrated using anterograde and retrograde tract tracers. The primary function of this innervation is lipid mobilization. The brain SNS outflow to WAT has been defined using the pseudorabies virus (PRV), a retrograde transneuronal tract tracer. These PRV-labelled SNS outflow neurons are extensively co-localized with melanocortin-4 receptor mRNA, which, combined with functional data, suggests their involvement in lipolysis. The SNS innervation of WAT also regulates fat cell number, as noradrenaline inhibits and WAT denervation stimulates fat cell proliferation in vitro and in vivo respectively. The sensory innervation of WAT has been demonstrated by retrograde tract tracing, electrophysiological recording and labelling of the sensory-associated neuropeptide calcitonin gene-related peptide in WAT. Local injections of the sensory nerve neurotoxin capsaicin into WAT selectively destroy this innervation. Just as surgical removal of WAT pads triggers compensatory increases in lipid accretion by non-excised WAT depots, capsaicin-induced sensory denervation triggers increases in lipid accretion of non-capsaicin-injected WAT depots, suggesting that these nerves convey information about body fat levels to the brain. Finally, parasympathetic nervous system innervation of WAT has been suggested, but the recent finding of no WAT immunoreactivity for the possible parasympathetic marker vesicular acetylcholine transporter (VAChT) argues against this claim. Collectively, these data suggest several roles for efferent and afferent neural innervation of WAT in body fat regulation.

Type
Symposium on ‘Biology of obesity’
Copyright
Copyright © The Nutrition Society 2005

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