β-adrenergic stimulation of fatty acid release from brown fat cells differentiated in monolayer culture

Kuusela, Pertti; Nedergaard, Jan; Cannon, Barbara

doi:10.1016/0024-3205(86)90052-4

Cited by 28 publications

(10 citation statements)

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“…Considering the fact that NA-induced thermogenesis also increases glucose uptake and utilization in BAT, we suggest that the lipid oxidation is lower as assumed and lipid loss may be even greater than 11 times as compared with metabolic rate ( 51,54 ). An exaggerated mobilization and export of fatty acids from adipocytes was also observed in vitro following noradrenergic stimulation ( 18,55,56 ). The in vitro observations suggest that the export of fatty acids is a native property of brown adipocyte metabolism.…”

Section: In Vivo Lipid Oxidation During Na-induced Thermogenesismentioning

confidence: 66%

Brown adipose tissue dynamics in wild-type and UCP1-knockout mice: in vivo insights with magnetic resonance

Grimpo

Völker

Heppe

et al. 2014

Journal of Lipid Research

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This article is available online at http://www.jlr.org body temperature maintenance of small eutherian mammals and newborns during periods of cold exposure. BAT thermogenesis is activated by the release of noradrenaline (NA) from sympathetic innervation. Uncoupling protein 1 (UCP1) in the inner mitochondrial membrane of the brown adipocytes uncouples the respiratory chain from ATP synthesis and thus energy is dissipated as heat ( 1-3 ). Prolonged cold exposure or a short photoperiod induces the recruitment of BAT ( 4-6 ). Brown adipocytes of coldadapted mice, contain small and multilocular lipid vacuoles, which are rich in cytoplasm and have a high content of mitochondrial protein (7)(8)(9). This provides an enhanced thermogenic capacity during cold exposure, and BAT can be considered as the major site of adaptive nonshivering thermogenesis (NST) in rodents and other small mammals ( 4, 10-12 ).The breakdown of lipids via lipoprotein lipase plays an important role during UCP1-mediated heat production ( 13 ). Free fatty acids (FFAs) directly activate UCP1 and feed the respiratory chain, i.e., FFAs are the major substrate for NST ( 14,15 ). Therefore active BAT is considered as a main consumer of lipids and FFAs and its contribution to plasma clearance of administered triglycerides has been shown previously ( 16,17 ). On the other hand a release of fatty acids during thermogenesis from BAT has been assumed, indicating a substrate supply to other tissues ( 18,19 ). Sympathetic activation by cold exposure or injections of NA not only activate BAT but also stimulate sympathetic receptors in general, leading to an increase in heart rate, blood flow, and metabolic responses in other tissues. The contribution of these UCP1-independent processes to total NST remain unclear ( 20, 21 ).Abstract We used noninvasive magnetic resonance imaging (MRI) and magnetic resonance spectroscopy to compare interscapular brown adipose tissue (iBAT) of wild-type (WT) and uncoupling protein 1 (UCP1)-knockout mice lacking UCP1-mediated nonshivering thermogenesis (NST). Mice were sequentially acclimated to an ambient temperature of 30°C, 18°C, and 5°C. We detected a remodeling of iBAT and a decrease in its lipid content in all mice during cold exposure. Ratios of energy-rich phosphates (ATP/ADP, phosphocreatine/ATP) in iBAT were maintained stable during noradrenergic stimulation of thermogenesis in coldand warm-adapted mice and no difference between the genotypes was observed. As free fatty acids (FFAs) serve as fuel for thermogenesis and activate UCP1 for uncoupling of oxidative phosphorylation, brown adipose tissue is considered to be a main acceptor and consumer of FFAs. We measured a major loss of FFAs from iBAT during noradrenergic stimulation of thermogenesis. This mobilization of FFAs was observed in iBAT of WT mice as well as in mice lacking UCP1. The high turnover and the release of FFAs from iBAT suggests an enhancement of lipid metabolism, which in itself contributes to the sympathetically activated NST and which is independent fro...

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Section: In Vivo Lipid Oxidation During Na-induced Thermogenesismentioning

confidence: 66%

Brown adipose tissue dynamics in wild-type and UCP1-knockout mice: in vivo insights with magnetic resonance

Grimpo

Völker

Heppe

et al. 2014

Journal of Lipid Research

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“…Lipolysis, observed as glycerol or fatty acid release, is norepinephrine-induced in brown adipocytes (51,206,419,568), just as is thermogenesis (208,562,630). Lipolysis is stimulated through ␤ 3 -receptors (25,124) as is FIG. 3.…”

Section: Stimulation Of Lipolysis Stimulates Thermogenesismentioning

confidence: 92%

Brown Adipose Tissue: Function and Physiological Significance

Cannon

Nedergaard

2004

Physiological Reviews

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5,550

126

5,981

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The function of brown adipose tissue is to transfer energy from food into heat; physiologically, both the heat produced and the resulting decrease in metabolic efficiency can be of significance. Both the acute activity of the tissue, i.e., the heat production, and the recruitment process in the tissue (that results in a higher thermogenic capacity) are under the control of norepinephrine released from sympathetic nerves. In thermoregulatory thermogenesis, brown adipose tissue is essential for classical nonshivering thermogenesis (this phenomenon does not exist in the absence of functional brown adipose tissue), as well as for the cold acclimation-recruited norepinephrine-induced thermogenesis. Heat production from brown adipose tissue is activated whenever the organism is in need of extra heat, e.g., postnatally, during entry into a febrile state, and during arousal from hibernation, and the rate of thermogenesis is centrally controlled via a pathway initiated in the hypothalamus. Feeding as such also results in activation of brown adipose tissue; a series of diets, apparently all characterized by being low in protein, result in a leptin-dependent recruitment of the tissue; this metaboloregulatory thermogenesis is also under hypothalamic control. When the tissue is active, high amounts of lipids and glucose are combusted in the tissue. The development of brown adipose tissue with its characteristic protein, uncoupling protein-1 (UCP1), was probably determinative for the evolutionary success of mammals, as its thermogenesis enhances neonatal survival and allows for active life even in cold surroundings.

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“…In the control conditions, cells presented a differentiated morphology with a high lipid droplet content and had the capacity to respond to a 10 -7 M NE treatment, showing the characteristic NE-activated morphology of differentiated brown adipocytes in culture due to an adrenergic lipolytic response [24], with much smaller and fewer lipid droplets than the non-NE-treated cells. For the Oil red O staining assay, hormone treatments were carried out only at the higher concentration presented in the rest of the experiments, i.e.…”

Section: Morphological Differences Of Brown Adipocytes In Culture Aftmentioning

confidence: 99%

Opposite actions of testosterone and progesterone on UCP1 mRNA expression in cultured brown adipocytes

Rodríguez¹,

Monjo²,

Roca³

et al. 2002

CMLS, Cell. Mol. Life Sci.

105

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The brown adipose tissue (BAT) thermogenic response to diet-induced obesity and cold has been found to be gender dependent. In the present work, we aimed to investigate the effects of the main physiological male and female sex hormones, i.e. testosterone, progesterone and 17-beta-estradiol, on the expression of uncoupling protein I (UCP1)--the main mediator of BAT thermogenesis--and on UCP2 and lipid accumulation in rodent brown adipocytes differentiated in culture. Testosterone-treated cells showed fewer and smaller lipid droplets than control cells and a dose-dependent inhibition of UCP1 mRNA expression, under adrenergic stimulation by norepinephrine (NE). These effects were reverted by the androgen receptor antagonist flutamide, suggesting they are dependent, at least in part, on the androgen receptor. Progesterone- and 17-beta-estradiol-treated cells showed more and larger lipid droplets and progesterone stimulated NE-induced UCP1 mRNA expression at the lower concentration tested, but not at higher concentrations, suggesting that for brown adipocytes, this hormone is dose dependent. 17-beta-Estradiol did not have any remarkable effect either on UCP1 or UCP2 mRNA expression. Interestingly, the specific progesterone receptor antagonist RU486 induced UCP1 and UCP2 mRNAs, including UCP1 mRNA expression in non-NE-treated brown adipocytes, suggesting a profound effect of this antiprogestagen on brown adipocyte thermogenic capacity. Thus, are conclude that testosterone, 17-beta-estradiol, progesterone and RU486 have distinct actions on brown adipocytes, thus modulating UCP1 and UCP2 mRNA expression and/or lipid accumulation, and that sex hormones are factors that may explain in part the gender-dependent BAT thermogenic response.

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β-adrenergic stimulation of fatty acid release from brown fat cells differentiated in monolayer culture

Cited by 28 publications

References 28 publications

Brown adipose tissue dynamics in wild-type and UCP1-knockout mice: in vivo insights with magnetic resonance

Brown adipose tissue dynamics in wild-type and UCP1-knockout mice: in vivo insights with magnetic resonance

Brown Adipose Tissue: Function and Physiological Significance

Opposite actions of testosterone and progesterone on UCP1 mRNA expression in cultured brown adipocytes

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