Sensory innervation of white adipose tissue

Fishman, Renata B.; Dark, John

doi:10.1152/ajpregu.1987.253.6.r942

Cited by 70 publications

(73 citation statements)

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“…Collectively, we present for the first time the central targets of WAT sensory afferents and demonstrate a condition that stimulates these afferents. Therefore, these data reinforce and greatly extend the seminal finding of the sensory innervation of WAT demonstrated over 20 years ago in a more limited manner when a traditional retrograde tract tracer injected into WAT-labeled DRG pseudounipolar neurons (18).…”

Section: Discussionsupporting

confidence: 84%

“…Sensory innervation of WAT was shown directly when a conventional retrograde tract tracer was applied to laboratory rat WAT, resulting in labeling of the pseudounipolar (a.k.a. bipolar) neurons of dorsal root ganglia (DRG) (18). In addition, while the present study was in progress, it was reported that injections of the cholera toxin b subunit (CTb) injections into rat retroperitoneal WAT suggest sensory nerve projections to the nucleus gracilis (Gr) of the brainstem (26).…”

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confidence: 73%

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Anterograde transneuronal viral tract tracing reveals central sensory circuits from white adipose tissue

Song¹,

Schwartz²,

Bartness³

2009

American Journal of Physiology-Regulatory, Integrative and Comp

120

131

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Song CK, Schwartz GJ, Bartness TJ. Anterograde transneuronal viral tract tracing reveals central sensory circuits from white adipose tissue. Am J Physiol Regul Integr Comp Physiol 296: R501-R511, 2009. First published December 24, 2008 doi:10.1152/ajpregu.90786.2008The origins of the sympathetic nervous system (SNS) innervation of white adipose tissue (WAT) have been defined using the transneuronal viral retrograde tract tracer, pseudorabies virus. Activation of this SNS innervation is acknowledged as the principal initiator of WAT lipolysis. The central control of WAT lipolysis may require neural feedback to a brain-SNS-WAT circuit via WAT afferents. Indeed, conventional tract tracing studies have demonstrated that peripheral pseudounipolar dorsal root ganglion (DRG) sensory cells innervate WAT. The central nervous system projections of WAT afferents remain uncharted, however, and form the focus of the present study. We used the H129 strain of the herpes simplex virus-1 (HSV-1), an anterograde transneuronal viral tract tracer, to define the afferent circuits projecting from WAT to the central nervous system. Siberian hamster inguinal (IWAT) or epididymal WAT was injected with H129 and the neuraxis processed for HSV-1 immunoreactivity. We found substantial overlap in the pattern of WAT sensory afferent projections with multiple SNS outflow sites along the neuraxis, suggesting the possibility of WAT sensory-SNS circuits that could regulate WAT SNS drive and thereby lipolysis. Previously, we demonstrated that systemic 2-deoxy-D-glucose (2DG) elicited increases in the SNS drive to IWAT. Here, we show that systemic 2DG administration also significantly increases multiunit spike activity arising from decentralized IWAT afferents. Collectively, these data provide structural and functional support for the existence of a sensory WAT pathway to the brain, important in the negative feedback control of lipid mobilization.2-deoxy-D-glucose; lipolysis; sympathetic nervous system; electrophysiology FEEDBACK FROM LIPID STORES to the central nervous system (CNS) has been suggested to contribute to the relative stability of total body fat in some individuals, but not in others (for a review, see Ref. 1). Historically, the idea of a lipid feedback signal became prominent with Kennedy's "lipostatic theory" (24), and this notion apparently was affirmed with the discovery of leptin, the largely adipocyte-derived cytokine thought by some to reflect total body fat stores (for a review, see Ref. 21). As with any feedback system, one controlling lipid stores would require not only afferent signals from white adipose tissue (WAT), but also effectors to increase or decrease the lipid stores appropriately. As with any feedback system, one controlling lipid stores would require not only afferent signals from WAT, but also effectors to increase or decrease the lipid stores appropriately. Whether such a system exists or needs to exist for total body fat to be stable is debatable (46). Efferent neural control of WAT is well recognized. We and...

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Section: Discussionsupporting

confidence: 84%

mentioning

confidence: 73%

Anterograde transneuronal viral tract tracing reveals central sensory circuits from white adipose tissue

Song¹,

Schwartz²,

Bartness³

2009

American Journal of Physiology-Regulatory, Integrative and Comp

120

131

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“…It can not be excluded that the effects of neonatal capsaicin-treatment on lipogenesis and plasma non-esterified fatty acid concentrations may result from a direct effect of capsaicin on adipose tissue sensory nerves. Consistent with this, it has been reported that inguinal and dorsal subcutaneous fat depots in rats contain sensory nerve terminals [29] which are sensitive to capsaicin.…”

Section: Discussionsupporting

confidence: 80%

Neonatal de-afferentation of capsaicin-sensitive sensory nerves increases in vivo insulin sensitivity in conscious adult rats

1998

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“…The sensory innervation of WAT is suggested by the existence of substance P and calcitonin gene-related peptide, typical marker peptides of primary sensory neurons 29 . Retrograde-tracing experiments also revealed that peripheral pseudounipolar dorsal root ganglion cells innervate WAT 30 . Song et al 31 further showed that afferent nerves in WAT project into many areas of brain, including the hypothalamus.…”

Section: Discussionmentioning

confidence: 89%

Possible involvement of uncoupling protein 1 in appetite control by leptin

Okamatsu‐Ogura

Nio‐Kobayashi

Iwanaga

et al. 2011

Exp Biol Med (Maywood)

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Leptin reduces body fat by decreasing food intake and increasing energy expenditure. Uncoupling protein (UCP) 1, a key molecule for brown adipose tissue (BAT) thermogenesis, was reported to contribute to the stimulatory effect of leptin on energy expenditure. To clarify whether UCP1 is also involved in the anorexigenic effect of leptin, in this study we examined the effect of leptin on food intake using wild-type (WT) and UCP1-deficient (UCP1-KO) mice. Repeated injection of leptin decreased food intake more markedly in WT mice than in UCP1-KO mice, while a single injection of leptin showed similar effects in the two groups of mice. As chronic leptin stimulation induces UCP1 expression in BAT and ectopically in white adipose tissue (WAT), we mimicked the UCP1 induction by repeated injection of CL316,243 (CL), a highly specific ß3-adrenoceptor agonist, and measured food intake in response to a single injection of leptin. Two-week treatment with CL enhanced the anorexigenic effect of leptin in WT mice, but not in UCP1-KO mice. Three-day treatment with CL in WT mice also enhanced the anorexigenic effect of leptin and leptin-induced phosphorylation of STAT3 in the arcuate nucleus of the hypothalamus, without any notable change in adiposity. These results indicate that UCP1 enhances leptin action at the hypothalamus level, suggesting UCP1 contributes to the control of energy balance not only through the regulation of energy expenditure, but also through appetite control by modulating leptin action.

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Sensory innervation of white adipose tissue

Cited by 70 publications

References 0 publications

Anterograde transneuronal viral tract tracing reveals central sensory circuits from white adipose tissue

Anterograde transneuronal viral tract tracing reveals central sensory circuits from white adipose tissue

Neonatal de-afferentation of capsaicin-sensitive sensory nerves increases in vivo insulin sensitivity in conscious adult rats

Possible involvement of uncoupling protein 1 in appetite control by leptin

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