The control of UCP1 is dissociated from that of PGC‐1α or of mitochondriogenesis as revealed by a study using β‐less mouse brown adipocytes in culture

Lehr, Lorenz; Canola, Kriss; Asensio, Cédric S.; Jiménez, María; Kuehne, Françoise; Giacobino, Jean‐Paul; Muzzin, Patrick

doi:10.1016/j.febslet.2006.07.037

Cited by 24 publications

(16 citation statements)

References 31 publications

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“…Concerning UCP1 in BAT, we observed that this parameter is lower in b-less than in WT animals, an observation in keeping with previously reported results. 27 As was observed in WT mice, food restriction had no effect on BAT UCP1 expression in b-less animals. The situation is different for BAT D2 expression, as we observed that food restriction failed to promote a decrease in this parameter in b-less mice as it does in WT mice.…”

Section: Control P-f Leptinsupporting

confidence: 51%

Effects of leptin on energy metabolism in β-less mice

Asensio¹,

Arsenijevic²,

Lehr³

et al. 2008

Int J Obes

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Objective: To investigate the impact of b-adrenoceptor deficiency on the metabolic effects of leptin. Measurements: Leptin was infused subcutaneously through an osmotic minipump in wild-type (WT) and b 1 /b 2 /b 3 -adrenoceptor knockout (b-less) mice and its effects on food intake, energy expenditure, carbohydrate and lipid utilization as well as on the levels of expression of the brown adipose tissue (BAT), thermogenic marker uncoupling protein-1 (UCP1) and type II deiodinase (D2) mRNAs were compared. Results: Leptin treatment decreased food intake by 23% in both the WT and the b-less mice. In pair-fed animals being used as controls, leptin treatment was found to increase energy expenditure in WT, but not in b-less mice. No difference was observed in carbohydrate or fat utilization between leptin-treated WT and b-less mice. Leptin increased UCP1 and D2 mRNA levels in WT mouse BAT 1.7-and 3-fold, respectively, but had no effect on the expression of these genes in b-less mouse BAT. Conclusion: The stimulatory effects of leptin on oxygen consumption, BAT UCP1 and D2 expression require functional b-adrenoceptors, but its inhibitory effect on food intake and its stimulatory effect on fat utilization is independent of the b-adrenoceptor signalling.

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Section: Control P-f Leptinsupporting

confidence: 51%

Effects of leptin on energy metabolism in β-less mice

Asensio¹,

Arsenijevic²,

Lehr³

et al. 2008

Int J Obes

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“…However, Petrovic et al (27) recently showed that a proportion of mitochondrion-rich cells are UCP-1 positive, whereas numerous mitochondrion-rich cells are negative for UCP-1 during the induction of brown adipocytes in WAT by PPAR-␥ activation. A recent study also showed that, in a primary culture of ␤-adrenoceptor knockout brown adipocytes, UCP-1 mRNA expression level is markedly decreased, whereas PGC-1␣ and TFAM mRNA expression levels are not (23). Moreover, in the same experiment, UCP-1, PGC-1␣, and COX IV protein expression levels are decreased by 97, 62, and 22%, respectively.…”

Section: Discussionmentioning

confidence: 63%

Triiodothyronine induces UCP-1 expression and mitochondrial biogenesis in human adipocytes

Lee

Takahashi

Yasubuchi³

et al. 2012

American Journal of Physiology-Cell Physiology

150

112

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Uncoupling protein (UCP)-1 expressed in brown adipose tissue plays an important role in thermogenesis. Recent data suggest that brown-like adipocytes in white adipose tissue (WAT) and skeletal muscle play a crucial role in the regulation of body weight. Understanding of the mechanism underlying the increase in UCP-1 expression level in these organs should, therefore, provide an approach to managing obesity. The thyroid hormone (TH) has profound effects on mitochondrial biogenesis and promotes the mRNA expression of UCP in skeletal muscle and brown adipose tissue. However, the action of TH on the induction of brown-like adipocytes in WAT has not been elucidated. Thus we investigate whether TH could regulate UCP-1 expression in WAT using multipotent cells isolated from human adipose tissue. In this study, triiodothyronine (T3) treatment induced UCP-1 expression and mitochondrial biogenesis, accompanied by the induction of the CCAAT/enhancer binding protein, peroxisome proliferator-activated receptor-γ coactivator-1α, and nuclear respiratory factor-1 in differentiated human multipotent adipose-derived stem cells. The effects of T3 on UCP-1 induction were dependent on TH receptor-β. Moreover, T3 treatment increased oxygen consumption rate. These findings indicate that T3 is an active modulator, which induces energy utilization in white adipocytes through the regulation of UCP-1 expression and mitochondrial biogenesis. Our findings provide evidence that T3 serves as a bipotential mediator of mitochondrial biogenesis.

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“…PPARγ coactivator 1α (PGC-1a) is a PPARγ interacting protein and is restricted to oxidative tissues including BAT and skeletal muscle [32]. It is observed that cold and /or adrenergic stimulation increases the expression of this gene in BAT and then induces elevated expression of UCP1 [33], [34]. The heart-type fatty acid-binding protein (FABP3) is essential for efficient brown adipose tissue fatty acid oxidation and cold tolerance.…”

Section: Discussionmentioning

confidence: 99%

Functional Evolution of Leptin of Ochotona curzoniae in Adaptive Thermogenesis Driven by Cold Environmental Stress

et al. 2011

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BackgroundEnvironmental stress can accelerate the directional selection and evolutionary rate of specific stress-response proteins to bring about new or altered functions, enhancing an organism's fitness to challenging environments. Plateau pika (Ochotona curzoniae), an endemic and keystone species on Qinghai-Tibetan Plateau, is a high hypoxia and low temperature tolerant mammal with high resting metabolic rate and non-shivering thermogenesis to cope in this harsh plateau environment. Leptin is a key hormone related to how these animals regulate energy homeostasis. Previous molecular evolutionary analysis helped to generate the hypothesis that adaptive evolution of plateau pika leptin may be driven by cold stress.Methodology/Principal FindingsTo test the hypothesis, recombinant pika leptin was first purified. The thermogenic characteristics of C57BL/6J mice injected with pika leptin under warm (23±1°C) and cold (5±1°C) acclimation is investigated. Expression levels of genes regulating adaptive thermogenesis in brown adipose tissue and the hypothalamus are compared between pika leptin and human leptin treatment, suggesting that pika leptin has adaptively and functionally evolved. Our results show that pika leptin regulates energy homeostasis via reduced food intake and increased energy expenditure under both warm and cold conditions. Compared with human leptin, pika leptin demonstrates a superior induced capacity for adaptive thermogenesis, which is reflected in a more enhanced β-oxidation, mitochondrial biogenesis and heat production. Moreover, leptin treatment combined with cold stimulation has a significant synergistic effect on adaptive thermogenesis, more so than is observed with a single cold exposure or single leptin treatment.Conclusions/SignificanceThese findings support the hypothesis that cold stress has driven the functional evolution of plateau pika leptin as an ecological adaptation to the Qinghai-Tibetan Plateau.

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The control of UCP1 is dissociated from that of PGC‐1α or of mitochondriogenesis as revealed by a study using β‐less mouse brown adipocytes in culture

Cited by 24 publications

References 31 publications

Effects of leptin on energy metabolism in β-less mice

Effects of leptin on energy metabolism in β-less mice

Triiodothyronine induces UCP-1 expression and mitochondrial biogenesis in human adipocytes

Functional Evolution of Leptin of Ochotona curzoniae in Adaptive Thermogenesis Driven by Cold Environmental Stress

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