Effect of acclimation temperature on the concentration of the mitochondrial ‘uncoupling’ protein measured by radioimmunoassay in mouse brown adipose tissue

Ashwell, Margaret; Jennings, G.; Richard, Denis; Stirling, Dorothy M.; Trayhurn, Paul

doi:10.1016/0014-5793(83)80740-6

Cited by 65 publications

(22 citation statements)

References 23 publications

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“…In the cold, the magnitude of increase in Ucp1 protein expression in BAT is dependent both on the temperature and on the duration of exposure (2,28,81). In the studies we included in this overview, the employed HFDs greatly vary in fat content between 30 and 82% of energy.…”

Section: Treatment Parametersmentioning

confidence: 99%

“…While this first surge seems to be maximal, even in response to mild cold exposure, mRNA levels after chronic cold exposure are rather proportional to ambient temperature (19). On the protein level Ucp1 expression strongly increases proportionally to the ambient temperature and to the duration of cold exposure (2,28). In analogy to this adaptive thermoregulatory response, we aimed to determine the characteristics of a possible alteration of Ucp1 expression upon feeding a HFD.…”

Section: Significance and Perspectivesmentioning

confidence: 99%

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Uncoupling protein 1 expression and high-fat diets

Fromme

Klingenspor

2011

American Journal of Physiology-Regulatory, Integrative and Comp

155

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Uncoupling protein 1 (Ucp1) is the key component of β-adrenergically controlled nonshivering thermogenesis in brown adipocytes. This process combusts stored and nutrient energy as heat. Cold exposure not only activates Ucp1-mediated thermogenesis to maintain normothermia but also results in adaptive thermogenesis, i.e., the recruitment of thermogenic capacity in brown adipose tissue. As a hallmark of adaptive thermogenesis, Ucp1 synthesis is increased proportionally to temperature and duration of exposure. Beyond this classical thermoregulatory function, it has been suggested that Ucp1-mediated thermogenesis can also be employed for metabolic thermogenesis to prevent the development of obesity. Accordingly, in times of excess caloric intake, one may expect a positive regulation of Ucp1. The general impression from an overview of the present literature is, indeed, an increased brown adipose tissue Ucp1 mRNA and protein content after feeding a high-fat diet (HFD) to mice and rats. The reported increases are very variable in magnitude, and the effect size seems to be independent of dietary fat content and duration of the feeding trial. In white adipose tissue depots Ucp1 mRNA is generally downregulated by HFD, indicating a decline in the number of interspersed brown adipocytes.

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Section: Treatment Parametersmentioning

confidence: 99%

Section: Significance and Perspectivesmentioning

confidence: 99%

Uncoupling protein 1 expression and high-fat diets

Fromme

Klingenspor

2011

American Journal of Physiology-Regulatory, Integrative and Comp

155

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“…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 ).…”

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confidence: 99%

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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“…However, an alternative possibility to direct importance of the phospholipid alterations is that they simply represent a secondary local adaptive response in the mitochondrial membrane to the increase in the concentration of UCP1, or to the increased catabolism and thermogenesis that it catalyzes. The concentration of UCP1 rises threefold in the cold in rodents, from about 3% to 9% of mitochondrial protein (3,31,59), and this change in abundance of a protein that occupies a significant area of the inner membrane might require compensatory changes in acyl chains to accommodate it.…”

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confidence: 99%