Hernández A, Obregón M J
Unidad de Endocrinología Molecular, Consejo Superior de Investigaciones Científicas, Madrid, Spain.
Am J Physiol. 1996 Jul;271(1 Pt 1):E15-23. doi: 10.1152/ajpendo.1996.271.1.E15.
Iodothyronine type II 5'-deiodinase (5'D-II) activities were studied in cultures of rat brown adipocytes. In the presence of serum, the adrenergically stimulated 5'D-II activities were very low. In the absence of serum, adenosine 3',5'-cyclic monophosphate (cAMP) analogues stimulated 5'D-II activity. Thyroxine (T4) inhibited these increases. Norepinephrine slightly increased 5'D-II activity in hypothyroid conditions, but 3,5,3'-triiodothyronine (T3) strongly potentiated the adrenergic stimulation of 5'D-II (20-fold). T3 amplification of the adrenergic stimulation was via beta-adrenergic receptors, specifically mimicked by beta3-agonists, but it was not observed using cAMP analogues. The stimulatory effect of T3 predominated over the inhibitory action of T4, increased with exposure to T3, and required de novo protein synthesis. The half-life of 5'D-II was 30 min, suggesting that stabilization of 5'D-II did not occur. The effect was only observed in differentiated adipocytes. Retinoic acid has similar although smaller effects than T3. In conclusion, the presence of T3 is required and strongly potentiates the noradrenergic stimulation of 5'D-II activity in rat brown adipocytes.
在大鼠棕色脂肪细胞培养物中研究了II型碘甲状腺原氨酸5'-脱碘酶（5'D-II）的活性。在有血清存在的情况下，肾上腺素能刺激的5'D-II活性非常低。在无血清的情况下，3',5'-环磷酸腺苷（cAMP）类似物刺激5'D-II活性。甲状腺素（T4）抑制这些增加。去甲肾上腺素在甲状腺功能减退的情况下略微增加5'D-II活性，但3,5,3'-三碘甲状腺原氨酸（T3）强烈增强了5'D-II的肾上腺素能刺激（20倍）。T3对肾上腺素能刺激的放大作用是通过β-肾上腺素能受体，具体由β3-激动剂模拟，但使用cAMP类似物时未观察到。T3的刺激作用超过了T4的抑制作用，随着暴露于T3而增加，并且需要从头合成蛋白质。5'D-II的半衰期为30分钟，表明未发生5'D-II的稳定化。该作用仅在分化的脂肪细胞中观察到。视黄酸具有与T3相似但较小的作用。总之，T3的存在是必需的，并且强烈增强了大鼠棕色脂肪细胞中5'D-II活性的去甲肾上腺素能刺激。
