Absence of paravascular nerve projection and cross-innervation in interscapular brown adipose tissues of mice

Watanabe, Jun; Mishiro, Kayo; Amatsu, T; Kanamura, Shinsuke

doi:10.1016/0165-1838(94)90173-2

Cited by 8 publications

(10 citation statements)

References 18 publications

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“…BAT is densely innervated by the SNS, and SNS-mediated BAT thermogenesis and TG clearance are controlled by an area within the preoptic chiasma/anterior hypothalamic nuclei (PO/AH), located in front of the third ventricle ( 60,61 ). Cooling of this area activates BAT ( 62,63 ), whereas warming suppresses its activity ( 64 ).…”

Section: Sympathetic Innervation Of Batmentioning

confidence: 99%

“…The signal is mediated through the VMH and medulla oblongata and then passes through the spinal cord until it reaches the relevant IML neurons ( 65 ). From the consequent stellate ganglia ( 12 ), thin unmyelinated nerve fi bers directly innervate and activate each brown adipocyte, resulting in a dense innervation of the interscapular BAT depot ( 12,61 ) ( Fig. 1 ).…”

Section: Sympathetic Innervation Of Batmentioning

confidence: 99%

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Sympathetic nervous system control of triglyceride metabolism: novel concepts derived from recent studies

Geerling

Boon

Kooijman

et al. 2014

Journal of Lipid Research

107

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Dyslipidemia is one of the classical risk factors for cardiovascular diseases (CVD) besides hypertension, type 2 diabetes, and smoking ( 1 ). Dyslipidemia is defi ned as an elevation of plasma LDL-cholesterol (LDL-C), triglycerides (TG), or both, with or without a lowering of HDLcholesterol (HDL-C) ( 2 ). Whereas elevated LDL-C is a well-established major predictor of CVD and has been the primary target for lipid-lowering strategies, evidence suggests that an elevated TG level is an independent risk factor for CVD development as well ( 3, 4 ). Plasma TG levels are considered elevated when they exceed 150 mg/dl, which is observed in 31% of the adult US population ( 5 ). Although hypertriglyceridemia can be caused by rare monogenic disorders, it is mostly caused by a complex interaction between environmental factors and subtle variations in genes involved in lipoprotein metabolism ( 5 ). Current treatments for hypertriglyceridemia are aimed at either increasing TG clearance (e.g., fi brates) ( 6 ) or at decreasing lipolysis in WAT (e.g., niacin) ( 7 ). In addition, reduction of VLDL-TG production lowers plasma TG levels (e.g., exendin-4) ( 8 ).In recent years, the autonomic nervous system, which consists of a sympathetic and a parasympathetic branch, emerged as an important regulator of metabolic homeostasis. Whereas the role of the sympathetic nervous system (SNS) in the regulation of glucose metabolism has been fi rmly established (for review, see Ref. 9 ), considerably fewer studies have focused on its role in TG metabolism. This review provides an update specifi cally on the role of Abstract Important players in triglyceride (TG) metabolism include the liver (production), white adipose tissue (WAT) (storage), heart and skeletal muscle (combustion to generate ATP), and brown adipose tissue (BAT) (combustion toward heat), the collective action of which determine plasma TG levels. Interestingly, recent evidence points to a prominent role of the hypothalamus in TG metabolism through innervating the liver, WAT, and BAT mainly via sympathetic branches of the autonomic nervous system. Here, we review the recent fi ndings in the area of sympathetic control of TG metabolism. Various neuronal populations, such as neuropeptide Y (NPY)-expressing neurons and melanocortin-expressing neurons, as well as peripherally produced hormones (i.e., GLP-1, leptin, and insulin), modulate sympathetic outfl ow from the hypothalamus toward target organs and thereby infl uence peripheral TG metabolism. We conclude that sympathetic stimulation in general increases lipolysis in WAT, enhances VLDL-TG production by the liver, and increases the activity of BAT with respect to lipolysis of TG, followed by combustion of fatty acids toward heat. Moreover, the increased knowledge about the involvement of the neuroendocrine system in TG metabolism presented in this review offers new therapeutic options to fi ght hypertriglyceridemia by specifi cally modulating sympathetic nervous system outfl ow toward liver, BAT, or WAT .-Geerling, J. J., M. R. B...

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Section: Sympathetic Innervation Of Batmentioning

confidence: 99%

Section: Sympathetic Innervation Of Batmentioning

confidence: 99%

Sympathetic nervous system control of triglyceride metabolism: novel concepts derived from recent studies

Geerling

Boon

Kooijman

et al. 2014

Journal of Lipid Research

107

View full text Add to dashboard Cite

show abstract

“…However, the failure of NPY to modulate the cAMP production, oxygen consumption and also ERK activation suggests that functional NPY receptors are lacking in brown adipocytes. Therefore, it is unlikely that NPY directly controls basal and NE-regulated thermogenesis in a short period of time, even if some sympathetic nerves carrying both NE and NPY innervate brown adipocytes [23,28,38].…”

Section: Discussionmentioning

confidence: 99%

“…The co-existence of sympathetic and peptidergic innervation has been demonstrated in BAT [5,11,23,28,38]. Among peptidergic neurotransmitters, neuropeptide Y (NPY) levels in the BAT are significantly decreased and increased by surgical excision of the sympathetic nerves to the BAT and putting an animal into a cold environment, respectively [30].…”

Section: Introductionmentioning

confidence: 99%

“…Similarly, it is suggested that NPY co-localizes with tyrosine hydroxylase in noradrenergic neurons, but only in the perivascular nerve fiber network [11]. However, other studies showed that NE-and NPY-positive fibers were also found around parenchymal brown adipocytes in mice [38] and rats [23,28]. 4 NPY exhibits its physiological effects through at least four receptors known as Y1, Y2, Y4, and Y5.…”

Section: Introductionmentioning

confidence: 99%

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