Thyroid-Hormone-Induced Browning of White Adipose Tissue Does Not Contribute to Thermogenesis and Glucose Consumption
Thyroid-Hormone-Induced Browning of White Adipose Tissue Does Not Contribute to Thermogenesis and Glucose Consumption
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DOI：
10.1016/j.celrep.2019.05.054
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发表时间：
2019-06-11
期刊：
影响因子：
8.8
通讯作者：
Mittag, Jens
中科院分区：
文献类型：
--
作者：
Johann, Kornelia;Cremer, Anna Lena;Mittag, Jens
体温的调节主要取决于甲状腺激素（TH）。最近的研究表明，TH诱导白色脂肪组织的布朗宁，可能导致甲亢患者中观察到的体温过高，并可能提供代谢益处。在这里，我们表明，布朗宁TH需要TH-受体β和交感神经系统独立发生。然而，米色脂肪缺乏足够的肾上腺素能刺激，尽管解偶联蛋白1（UCP 1）水平高，但没有代谢活化。在不同环境温度下的研究表明，TH通过骨骼肌中的作用结合中心体温设定点升高而引起体温过高。因此，在UCP 1敲除小鼠中维持了全身性甲状腺功能亢进症的代谢和产热效应，表明米色或棕色脂肪均不会导致TH诱导的体温过高和葡萄糖消耗增加，并强调仅存在UCP 1不足以得出关于布朗宁剂治疗潜力的结论。
Regulation of body temperature critically depends on thyroid hormone (TH). Recent studies revealed that TH induces browning of white adipose tissue, possibly contributing to the observed hyperthermia in hyperthyroid patients and potentially providing metabolic benefits. Here, we show that browning by TH requires TH-receptor beta and occurs independently of the sympathetic nervous system. The beige fat, however, lacks sufficient adrenergic stimulation and is not metabolically activated despite high levels of uncoupling protein 1 (UCP1). Studies at different environmental temperatures reveal that TH instead causes hyperthermia by actions in skeletal muscle combined with a central body temperature set-point elevation. Consequently, the metabolic and thermo-genic effects of systemic hyperthyroidism were maintained in UCP1 knockout mice, demonstrating that neither beige nor brown fat contributes to the TH-induced hyperthermia and elevated glucose consumption, and underlining that the mere presence of UCP1 is insufficient to draw conclusions on the therapeutic potential of browning agents.