Abstract
During our study of the reversal of seasonal obesity in Siberian hamsters, we found an interaction between receptors for the pineal hormone melatonin and the sympathetic nervous system (SNS) outflow from brain to white adipose tissue (WAT). This ultimately led us and others to conclude that the SNS innervation of WAT is the primary initiator of lipid mobilization in these as well as other animals, including humans. There is strong neurochemical (norepinephrine turnover), neuroanatomical (viral tract tracing), and functional (sympathetic denervation-induced blockade of lipolysis) evidence for the role of the SNS in lipid mobilization. Recent findings suggest the presence of WAT sensory innervation based on strong neuroanatomical (viral tract tracing, immunohistochemical markers of sensory nerves) and suggestive functional (capsaicin sensory denervation-induced WAT growth) evidence, the latter implying a role in conveying adiposity information to the brain. By contrast, parasympathetic nervous system innervation of WAT is characterized by largely negative neuroanatomical evidence (viral tract tracing, immunohistochemical and biochemical markers of parasympathetic nerves). Functional evidence (intraneural stimulation and in situ microdialysis) for the role of the SNS innervation in lipid mobilization in human WAT is convincing, with some controversy regarding the level of sympathetic nerve activity in human obesity.
Highlights
During our study of the reversal of seasonal obesity in Siberian hamsters, we found an interaction between receptors for the pineal hormone melatonin and the sympathetic nervous system (SNS) outflow from brain to white adipose tissue (WAT)
In the process of conducting this work, we discovered the importance of the sympathetic nervous system (SNS) in lipid mobilization from white adipose tissue (WAT) as well as more recently realizing the possible importance of the sensory innervation of WAT
This should not be misconstrued as a dismissal of “viscerotopic” sympathetic innervation of WAT at some point(s) across the neuroaxis; unequivocal demonstration of the viscerotopic organization of WAT circuitries requires careful studies using isogenic strains of the pseudorabies virus (PRV), each with unique fluorescent or other reporter injected into separate WAT pads [54]
Summary
Because of the largely negative nature of studies testing for the hormonal mediation of SD-induced decreases in adiposity in Siberian hamsters, we tested the role of adrenal medulla-secreted epinephrine (EPI). There were some differences in the degrees of infection (i.e., neurons participating in the circuit) at several sites across the neural axis among these WAT pads in Siberian hamsters, the general patterns of infection were more similar than different for the same WAT depots between Siberian hamsters and laboratory rats [62, 63] This should not be misconstrued as a dismissal of “viscerotopic” sympathetic innervation of WAT at some point(s) across the neuroaxis (see above for evidence of preganglionic and postganglionic viscerotopic patterns of sympathetic nerves innervating WAT); unequivocal demonstration of the viscerotopic organization of WAT circuitries requires careful studies using isogenic strains of the PRV, each with unique fluorescent or other reporter injected into separate WAT pads [54]. THE EXACT CIRCUITS AND BRAIN SITES RESPONSIBLE FOR ORCHESTRATING THE PHOTOPERIOD-INDUCED CHANGES IN BODY FAT ARE NOT KNOWN, BUT SOME LIKELY CANDIDATES
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