Silva J E, Larsen P R
Am J Physiol. 1986 Dec;251(6 Pt 1):E639-43. doi: 10.1152/ajpendo.1986.251.6.E639.
Norepinephrine, isoproterenol, insulin, and glucagon increase the type II (low Km) iodothyronine 5'-deiodinase (5'-D) in the brown adipose tissue (BAT) of intact rats. Cycloheximide or actinomycin D blocks the increase after norepinephrine, suggesting new mRNA synthesis is required for this effect. The 3- to 10-fold increase in BAT 5'-D after insulin administration was also blocked by cycloheximide. The effects of all stimulators are blunted by fasting or streptozotocin-induced diabetes. While all these hormones have the potential for stimulating BAT 5'-D, the dose-response relationships suggest that norepinephrine and insulin are the most potent. These and our earlier studies showing additional effects of thyroid and growth hormones on BAT 5'-D point to the complex regulation of this enzyme, suggesting that the triiodothyronine produced from its action has an important role in the thermogenic response of this tissue.
去甲肾上腺素、异丙肾上腺素、胰岛素和胰高血糖素可增加完整大鼠棕色脂肪组织(BAT)中的II型(低Km)碘甲状腺原氨酸5'-脱碘酶(5'-D)。放线菌酮或放线菌素D可阻断去甲肾上腺素作用后的增加,提示此效应需要新的mRNA合成。胰岛素给药后BAT 5'-D增加3至10倍的效应也被放线菌酮阻断。禁食或链脲佐菌素诱导的糖尿病会减弱所有刺激物的作用。虽然所有这些激素都有刺激BAT 5'-D的潜力,但剂量反应关系表明去甲肾上腺素和胰岛素最为有效。这些以及我们早期的研究表明甲状腺激素和生长激素对BAT 5'-D有额外作用,这表明该酶的调节很复杂,提示其作用产生的三碘甲状腺原氨酸在该组织的产热反应中起重要作用。