Thyroid hormone-sympathetic interaction and adaptive thermogenesis are thyroid hormone receptor isoform-specific
Thyroid hormone-sympathetic interaction and adaptive thermogenesis are thyroid hormone receptor isoform-specific
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DOI：
10.1172/jci200112584
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发表时间：
2001-07-01
影响因子：
15.9
通讯作者：
Brent, GA
中科院分区：
文献类型：
--
作者：
Ribeiro, MO;Carvalho, SD;Brent, GA
在新生儿和小型动物中，冷诱导的适应性（或非寒战）产热主要在棕色脂肪组织（BAT）中产生。产生热量是由交感神经系统刺激的，但它绝对需要甲状腺激素。我们使用甲状腺激素受体- β -选择性（TR- β -选择性）配体GC-1，通过药理学方法确定适应性产热是否具有TR异构体特异性，用不同剂量的T3或GC-1治疗甲状腺功能减退小鼠10天。解偶联蛋白1 （uncoupling protein 1, UCP1）是BAT的关键产热蛋白，在T3或GC-1处理下均能恢复其水平。然而，t3处理小鼠的肩胛间BAT在注射非肾上腺素后升高3.0℃，表明产热正常，但温度没有升高(
In newborns and small tnammals, cold-induced adaptive (or nonshivering) thermogenesis is produced primarily in brown adipose tissue (BAT). Heat production is stimulated by the sympathetic nervous system, but it has an absolute requirement for thyroid hormone. We used the thyroid hormone receptor-beta -selective (TR-beta -selective) ligand, GC-1, to determine by a pharmacological approach whether adaptive thermogenesis was TR isoform-specific, Hypothyroid mice were treated for 10 days with varying doses of T3 or GC-1. The level of uncoupling protein 1 (UCP1), the key thermogenic protein in BAT, was restored by either T3 or GC-1 treatment. However, whereas interscapular BAT in T3-treated mice showed a 3.0 degreesC elevation upon infusion of not epinephrine, indicating normal thermogenesis, the temperature did not increase (