Control of white and brown adipose tissues by the autonomic nervous system

Trayhurn, Paul; Ashwell, Margaret

doi:10.1079/pns19870017

Cited by 54 publications

(30 citation statements)

References 31 publications

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“…A recent study showed that activation of the hypothalamic-adipocyte axis promotes a phenotypic switch of scWAT to a brown-like adipose tissue (30). Since deletion of p22 phox in the PVN was associated with a significant reduction in WAT in the face of HFD (Figure 3, A-C), we speculated that browning and lipolysis of WAT may be involved (9). Markers of WAT browning including Ucp-1, Pgc-1α, and PR-domain-containing 16 (Prdm16) (30)(31)(32) were evaluated in scWAT.…”

Section: Selective Deletion Of P22mentioning

confidence: 99%

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Deletion of p22phox-dependent oxidative stress in the hypothalamus protects against obesity by modulating β3-adrenergic mechanisms

et al. 2017

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Section: Selective Deletion Of P22mentioning

confidence: 99%

“…Sympathetic stimulation of WAT induces breakdown of triacylglycerol via hormone-sensitive lipase (9). Recent studies show that increased norepinephrine in WAT induces expression of uncoupling protein 1 (Ucp1) and increases metabolic activity (10).…”

Section: Introductionmentioning

confidence: 99%

Deletion of p22phox-dependent oxidative stress in the hypothalamus protects against obesity by modulating β3-adrenergic mechanisms

et al. 2017

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“…Some of the factors or stimuli which could affect movement along the spectrum are genetic, hormonal, neural, physiological, pathological and nutritional. Evidence for the involvement of these factors is discussed in detail elsewhere Trayhurn & Ashwell, 1987;Trayhurn, 1990).…”

Section: Is There a Continuous Spectrum Of T H E Adipose Tissues?mentioning

confidence: 99%

Why do people get fat: is adipose tissue guilty?

Ashwell

1992

Proc. Nutr. Soc.

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“…Brown adipose tissue is known to be under the peripheral neurogenic control of the sympathetic nervous system (Landsberg,MS 8775 D. M. FYDA, K. E. COOPER AND W. L. VEALE Saville & Young, 1984;Trayhurn & Ashwell, 1987). Specifically, the release of noradrenaline from sympathetic nerve terminals activates fl-adrenergic receptors located on brown adipocytes to cause an increase in both oxygen consumption (Foster, 1985;Mohell, Connolly & Nedergaard, 1987) and local tissue temperature (Perkins, Rothwell, Stock, & Stone, 1981).…”

Section: Introductionmentioning

confidence: 99%

“…Specifically, the release of noradrenaline from sympathetic nerve terminals activates fl-adrenergic receptors located on brown adipocytes to cause an increase in both oxygen consumption (Foster, 1985;Mohell, Connolly & Nedergaard, 1987) and local tissue temperature (Perkins, Rothwell, Stock, & Stone, 1981). In addition, there is mounting evidence suggesting that ax-adrenoceptors, also located on brown fat cells, may play a synergistic role with the fl-receptors in mediating this non-shivering thermogenesis (Foster, 1985;Mohell et al 1987;Trayhurn & Ashwell, 1987).…”

Section: Introductionmentioning

confidence: 99%

Nucleus tractus solitarii lesions alter the metabolic and hyperthermic response to central prostaglandin E1 in the rat.

Fyda¹,

Cooper²,

Veale³

1991

The Journal of Physiology

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SUMMARY1. Given that the nucleus tractus solitarii (NTS) may regulate the ability of brown adipose tissue to evoke non-shivering thermogenesis and that brown fat may mediate the rise in whole-body metabolism observed following central pyrogen administration, we assessed whether interruption of baroreceptor afferents coursing though the NTS would interfere with the ability of prostaglandin E1 to evoke a normal fever response profile.2. Infusion of 150-600 ng of prostaglandin E1 (PGE1) into a lateral cerebral ventricle of the conscious rat resulted in a rise in core temperature, and also an increase in whole-body metabolic rate, brown adipose tissue temperature, arterial blood pressure and heart rate.3. Following bilateral electrolytic lesions to the NTS, resting core and brown fat temperatures, metabolic rates, blood pressures and heart rates in the NTS-lesioned animals were comparable to control rats. However, the PGE,-evoked increase in metabolic rate, along with the rise in core and brown adipose tissue temperatures and heart rate were attenuated. The pressor response was, however, enhanced, possibly due to the demonstrated interference by the lesions with normal baroreflex control.4. The findings suggest that the nucleus tractus solitarii region of the rats' brain may be important in mediating the thermogenesis evoked by central PGE1.

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Control of white and brown adipose tissues by the autonomic nervous system

Cited by 54 publications

References 31 publications

Deletion of p22phox-dependent oxidative stress in the hypothalamus protects against obesity by modulating β3-adrenergic mechanisms

Deletion of p22phox-dependent oxidative stress in the hypothalamus protects against obesity by modulating β3-adrenergic mechanisms

Why do people get fat: is adipose tissue guilty?

Nucleus tractus solitarii lesions alter the metabolic and hyperthermic response to central prostaglandin E1 in the rat.

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