Triiodothyronine induces UCP-1 expression and mitochondrial biogenesis in human adipocytes
Triiodothyronine induces UCP-1 expression and mitochondrial biogenesis in human adipocytes
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DOI：
10.1152/ajpcell.00010.2011
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发表时间：
2012-01-01
影响因子：
5.5
通讯作者：
Kawada, Teruo
中科院分区：
文献类型：
--
作者：
Lee, Joo-Young;Takahashi, Nobuyuki;Kawada, Teruo
Lee JY，Takahashi N，Yasubuchi M，Kim YI，Hashizaki H，Kim MJ，Sakamoto T，后藤T，Kawada T.三碘甲状腺原氨酸诱导人脂肪细胞UCP-1表达和线粒体生物合成。Am J Physiol Cell Physiol 302：C463-C472，2012.首次发表于2011年11月9日; doi：10.1152/ajpcell.00010.2011。解偶联蛋白-1在棕色脂肪组织中表达，在产热过程中起重要作用。最近的数据表明，在白色脂肪组织（WAT）和骨骼肌中的棕色样脂肪细胞在体重调节中起着至关重要的作用。因此，了解这些器官中UCP-1表达水平增加的机制应该提供一种控制肥胖的方法。甲状腺激素（TH）对骨骼肌和棕色脂肪组织线粒体的生物合成有重要影响，并促进UCP mRNA的表达。然而，TH对WAT中棕色样脂肪细胞诱导的作用尚未阐明。因此，我们调查是否TH可以调节UCP-1的表达在WAT使用多能细胞分离自人类脂肪组织。在这项研究中，三碘甲状腺原氨酸（T-3）治疗诱导UCP-1的表达和线粒体生物合成，伴随着诱导的CCAAT/增强子结合蛋白，过氧化物酶体增殖物激活受体-γ共激活因子-1 α，和核呼吸因子-1在分化的人多能脂肪源性干细胞。T-3对UCP-1诱导的作用依赖于TH受体β。此外，T-3处理增加耗氧速率。这些结果表明，T-3是一种主动调节剂，其通过调节UCP-1表达和线粒体生物合成来诱导白色脂肪细胞的能量利用。我们的研究结果提供了证据，T-3作为线粒体生物发生的双电位介质。
Lee JY, Takahashi N, Yasubuchi M, Kim YI, Hashizaki H, Kim MJ, Sakamoto T, Goto T, Kawada T. Triiodothyronine induces UCP-1 expression and mitochondrial biogenesis in human adipocytes. Am J Physiol Cell Physiol 302: C463-C472, 2012. First published November 9, 2011; doi:10.1152/ajpcell.00010.2011.-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 (T-3) treatment induced UCP-1 expression and mitochondrial biogenesis, accompanied by the induction of the CCAAT/enhancer binding protein, peroxisome proliferator-activated receptor-gamma coactivator-1 alpha, and nuclear respiratory factor-1 in differentiated human multipotent adipose-derived stem cells. The effects of T-3 on UCP-1 induction were dependent on TH receptor-beta. Moreover, T-3 treatment increased oxygen consumption rate. These findings indicate that T-3 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 T-3 serves as a bipotential mediator of mitochondrial biogenesis.