D'Agostino J, Henning S J
Am J Physiol. 1981 Apr;240(4):E402-6. doi: 10.1152/ajpendo.1981.240.4.E402.
The hormonal regulation of the ontogenic rise in serum corticosteroid-binding globulin (CBG) has been studied in the rat. Pups received daily injections of estrogens (either estradiol, estrone, or diethylstilbesterol, each at 0.05 microgram/g body wt) or thyroxine (0.1 microgram/g body wt) on postnatal days 2-7. When CBG binding capacity was determined on day 8, only the thyroxine-injected pups were found to have elevated CBG. This effect of thyroxine on CBG binding capacity was further studied by daily administration of the hormone (0.1 microgram.g body wt-1.day-1) between postnatal days 5-12. This caused a precocious rise in serum CBG, with CBG values 6- to 38-fold higher than euthyroid controls on days 8, 10, and 12. Conversely, in pups made hypothyroid by administration of propylthiouracil, the normal ontogenic increase in CBG was suppressed. Thyroxine replacement resulted in the reappearance of the CBG rise. These results suggest that the developmental rise in the binding capacity of CBG is independent of estradiol and estrone and instead is elicited by the rising concentrations of circulating thyroxine that normally occur in the early postnatal period.
在大鼠中研究了血清皮质类固醇结合球蛋白(CBG)个体发育性升高的激素调节。幼崽在出生后第2至7天每天注射雌激素(雌二醇、雌酮或己烯雌酚,每种剂量为0.05微克/克体重)或甲状腺素(0.1微克/克体重)。在第8天测定CBG结合能力时,发现只有注射甲状腺素的幼崽CBG升高。通过在出生后第5至12天每天给予甲状腺素(0.1微克·克体重-1·天-1)进一步研究了甲状腺素对CBG结合能力的影响。这导致血清CBG提前升高,在第8、10和12天,CBG值比甲状腺功能正常的对照组高6至38倍。相反,通过给予丙硫氧嘧啶使幼崽甲状腺功能减退,CBG的正常个体发育性增加受到抑制。甲状腺素替代导致CBG升高再次出现。这些结果表明,CBG结合能力的发育性升高与雌二醇和雌酮无关,而是由出生后早期正常出现的循环甲状腺素浓度升高引起的。