Glucocorticoids and hypothyroidism modulate development of fetal lung insulin receptors.
Glucocorticoids and hypothyroidism modulate development of fetal lung insulin receptors.
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糖皮质激素和甲状腺功能减退症调节胎儿肺胰岛素受体的发育。
DOI：
10.1152/ajpendo.1982.242.6.e384
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发表时间：
1982
期刊：
影响因子：
--
通讯作者：
Sperling,MA
中科院分区：
文献类型：
--
作者：
Devaskar,SU;Ganguli,S;Devaskar,UP;Sperling,MA
我们研究了正常个体发育期间胎兔肺膜中胰岛素受体的发育以及糖皮质激素和甲状腺功能减退症的影响。 125I-胰岛素与胎儿肺膜的特异性结合逐渐增加，在妊娠29天时达到峰值，随后下降30天。 Scatchard 图呈曲线状，显示受体数量（X 10(10)/mg 蛋白质）从 22-24 天的 129 +/- 7（平均值 +/- SE）逐渐增加到 29 天的 575 +/- 16，在 30 天时下降到 467 +/- 12，期限约为 31 天。亲和力在整个妊娠期间没有变化，并且与成人肺的亲和力相似； 26-30 天时，成人的受体数量显着低于胎儿。肾上腺素和 PGE1 可以使成人和胎儿肺膜中的 cAMP 产量增加一倍，直至 29 天。随着第 30 天胎儿胰岛素受体数量的下降，肾上腺素或 PGE1 产生的 cAMP 产量增加了五倍。胎儿甲状腺功能减退症的诱导使 28 天胎儿肺部的胰岛素受体数量比对照组减少了 70%（P 小于 0.001），而受体亲和力没有变化。相比之下，服用倍他米松可使胎儿肺胰岛素受体数量增加 250%（P 小于 0.001），但并未改变其亲和力；母体肺胰岛素受体没有改变。因此，胎儿肺胰岛素受体的正常个体发育的特征是数量逐渐增加，随后在临产前下降，与膜的 cAMP 反应性急剧增加相关。甲状腺功能减退症和糖皮质激素暴露可以调节胎儿肺胰岛素受体的正常发育。
We investigated the development of insulin receptors in membranes of fetal rabbit lung during normal ontogeny and the effect of glucocorticoids and hypothyroidism. Specific binding of 125I-insulin to fetal lung membranes increased progressively to a peak at 29 days gestation, declining by 30 days. Scatchard plots were curvilinear and revealed a progressive increase in receptor numbers (X 10(10)/mg protein) from 129 +/- 7 (mean +/- SE) at 22-24 days to 575 +/- 16 at 29 days, declining to 467 +/- 12 at 30 days, term being approximately 31 days. Affinities did not change throughout gestation and were similar to those of adult lung; receptor numbers in adults were significantly lower than in fetuses at 26-30 days. Epinephrine and PGE1 could evoke a doubling of cAMP production in adult and fetal lung membranes until 29 days. Concomitantly with the fall in fetal insulin receptor number at 30 days, cAMP production in response to epinephrine or PGE1 increased fivefold. Induction of fetal hypothyroidism decreased insulin receptor numbers in the lung of the 28-day fetus by 70% from control (P less than 0.001) without a change in receptor affinity. In contrast, betamethasone administration increased fetal lung insulin receptor numbers by 250% (P less than 0.001) but did not alter their affinity; maternal lung insulin receptors were not altered. Thus, normal ontogeny of the fetal lung insulin receptor is characterized by a progressive increase in number followed by decline immediately before parturition associated with a sharp increase of cAMP responsiveness of the membranes. Hypothyroidism and glucocorticoid exposure can modulate the normal development of the fetal lung insulin receptor.
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DOI：
--
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