Brown adipose tissue thermogenesis is activated by electrical and chemical (l-glutamate) stimulation of the ventromedial hypothalamic nucleus in cold-acclimated rats

Halvorson, I.; Gregor, L.; Thornhill, J. A.

doi:10.1016/0006-8993(90)91579-6

Cited by 26 publications

(12 citation statements)

References 9 publications

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“…Also, the VMH is thought to control BAT activation and thermogenesis (Halvorson et al, 1990; Lopez et al, 2010; Martinez de Morentin et al, 2014; Morrison et al, 2014). Importantly, Adrb3 expression levels are significantly increased in BAT from Sf1-Cre , Bmal1 loxP/loxP mice (Figure 4D), suggesting the implication of the SNS-BAT pathway in increased thermogenic capacity of these mice (Liew et al, 2013).…”

Section: Resultsmentioning

confidence: 99%

The Circadian Clock in the Ventromedial Hypothalamus Controls Cyclic Energy Expenditure

et al. 2016

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Organismal homeostasis relies on coherent interactions among tissues, specifically between brain-driven functions and peripheral metabolic organs. Hypothalamic circuits compute metabolic information to optimize energetic resources, but the role of the circadian clock in these pathways remains unclear. We have generated mice with targeted ablation of the core-clock gene Bmal1 within Sf1-neurons of the ventromedial hypothalamus (VMH). While this mutation does not affect the central clock in the suprachiasmatic nucleus (SCN), the VMH clock controls cyclic thermogenesis in brown adipose tissue (BAT), a tissue that governs energy balance by dissipating chemical energy as heat. VMH-driven control is exerted through increased adrenergic signaling within the sympathetic nervous system, without affecting the BAT’s endogenous clock. Moreover, we show that the VMH circadian clock computes light and feeding inputs to modulate basal energy expenditure. Thus, we reveal a previously unsuspected circuit where an SCN-independent, hypothalamic circadian clock controls BAT function, energy expenditure and thermogenesis.

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Section: Resultsmentioning

confidence: 99%

The Circadian Clock in the Ventromedial Hypothalamus Controls Cyclic Energy Expenditure

et al. 2016

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“…Conversely, inactivation of hypothalamic fatty acid metabolism reduces activation of BAT and prevents the weight loss associated with hyperthyroidism. To determine the physiological relevance of these observations, we investigated whether selective alteration of fatty acid metabolism in the VMH is sufficient to modulate BAT function 5, 44-46. We demonstrate that inactivation of AMPK in the VMH activates thermogenesis in BAT through the SNS.…”

Section: Discussionmentioning

confidence: 97%

Hypothalamic AMPK and fatty acid metabolism mediate thyroid regulation of energy balance

López

Varela

Vázquez

et al. 2010

Nat Med

605

719

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Thyroid hormones have widespread cellular effects; however it is unclear whether their effects on the central nervous system (CNS) contribute to global energy balance. Here, we demonstrate that either whole body hyperthyroidism or central administration of triiodothyronine (T3) decreases the activity of hypothalamic AMP-activated protein kinase (AMPK), increases sympathetic nervous system (SNS) activity and upregulates thermogenic markers in brown adipose tissue (BAT). Inhibition of the lipogenic pathway in the ventromedial nucleus of the hypothalamus (VMH) prevents CNS-mediated activation of BAT by thyroid hormone and reverses the weight loss associated with hyperthyroidism. Similarly inhibition of thyroid hormone receptors (TRs) in the VMH reverses the weight loss associated with hyperthyroidism. This regulatory mechanism depends on AMPK inactivation as genetic ablation of this enzyme in the VMH of euthyroid rats induces feeding-independent weight loss and increases expression of thermogenic markers in BAT. These effects are reversed by pharmacological blockade of the SNS. Thus, thyroid-hormone-induced modulation of AMPK activity and lipid metabolism in the hypothalamus is an important regulator of energy homeostasis.

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“…In addition, resting metabolic rate in MSG-treated laboratory mice (Poon and Cameron, 1978), and colonic temperature and total energy expenditure in MSG-treated rats (Schoelch et al, 2002; Yehuda et al, 1991) are significantly decreased compared with controls suggesting possible contribution of decreased thermogenesis to the development of the MSG-triggered obesity in our study. Because T b and T IBAT can be dissociated (Halvorson et al, 1990; Kobayashi et al, 1999; Madden and Morrison, 2009; Zaretskaia et al, 2002), we can only speculate that decreased T b contributed to the production of MSG-induced obesity in our animals because we did not measure T b here.…”

Section: Discussionmentioning

confidence: 99%

Acute brown adipose tissue temperature response to cold in monosodium glutamate-treated Siberian hamsters

Leitner

Bartness

2009

Brain Research

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Neonatal monosodium glutamate (MSG) administration increases adiposity, decreases energy expenditure and is associated with arcuate nucleus (Arc) destruction. Disrupted brown adipose tissue (BAT) thermogenesis underlies some of these effects, although, interscapular BAT temperature (T IBAT ) has not been measured. Therefore, we tested the effects of neonatal MSG or vehicle administration in Siberian hamsters and, when they were adults, measured T IBAT during acute cold exposure. The Arc and its projection to the hypothalamic paraventricular nucleus (PVH) are both components of the CNS outflow circuits to IBAT, with the latter implicated in BAT thermogenesis that could be compromised by MSG treatment. Using a viral transneuronal tract tracer, pseudorabies virus (PRV), we also tested whether the components of these circuits were intact. As adults, MSG-treated hamsters had significantly increased body mass and some white fat pad masses, markedly reduced Arc Nissl and neuropeptide staining, and PVH neuropeptide fiber staining. Cold-exposed (18 h at 5 °C) MSG-and vehicle-treated hamsters initially maintained T IBAT , but the ability of the former waned after 2 h being significantly decreased by 18 h. PRV immunoreactive fibers/cells were not altered by neonatal MSG treatment despite substantial Arc and PVH destruction. MSG-and vehicle-treated hamsters given an exogenous norepinephrine challenge showed identical increases in the duration and peak of T IBAT . Thus, the inability of MSG-treated animals to sustain T IBAT in the cold is not due to any obvious MSG-induced deletions of central sympathetic outflow circuits to IBAT, but appears to be extrinsic to the tissue nevertheless.

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Brown adipose tissue thermogenesis is activated by electrical and chemical (l-glutamate) stimulation of the ventromedial hypothalamic nucleus in cold-acclimated rats

Cited by 26 publications

References 9 publications

The Circadian Clock in the Ventromedial Hypothalamus Controls Cyclic Energy Expenditure

The Circadian Clock in the Ventromedial Hypothalamus Controls Cyclic Energy Expenditure

Hypothalamic AMPK and fatty acid metabolism mediate thyroid regulation of energy balance

Acute brown adipose tissue temperature response to cold in monosodium glutamate-treated Siberian hamsters

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