INFLUENCE OF HIGH-DENSITY LIPOPROTEIN ON ESTRADIOL STIMULATION OF LUTEAL STEROIDOGENESIS
INFLUENCE OF HIGH-DENSITY LIPOPROTEIN ON ESTRADIOL STIMULATION OF LUTEAL STEROIDOGENESIS
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DOI：
10.1095/biolreprod32.1.96
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发表时间：
1985-01-01
影响因子：
3.6
通讯作者：
GIBORI, G
中科院分区：
文献类型：
--
作者：
KHA, I;BELANGER, A;GIBORI, G
本研究的目的是确定黄体细胞是否利用来自高密度脂蛋白（HDL）的胆固醇进行类固醇合成，以及雌激素是否增强黄体对外源性固醇的利用。孵育第15天的黄体（CL）与不同剂量的人HDL导致剂量依赖性增加孕酮的生产。HDL在体外增强整体类固醇生成能力。然而，在17 α-羟孕酮、睾酮和雌二醇显著低于孕酮。第12天，切除垂体和垂体后叶的妊娠大鼠接受雌二醇、睾酮或溶剂处理72小时。类固醇治疗显著增加血清中的双烯醇酮和孕酮，但在体外生产的孕酮在所有组中的CL是相似的。然而，在介质中的HDL的存在下，只有黄体组织类固醇治疗的大鼠增加其孕酮输出。孕激素的产生减少的黄体细胞的车辆治疗的大鼠是不是由于累积的异羟孕酮，但在外源性甾醇利用的整体减少。结果表明，妊娠大鼠的黄体细胞有效地利用胆固醇从HDL的最大类固醇生成，雌二醇可能会刺激黄体类固醇生成，至少部分，通过影响HDL的胆固醇的掺入或利用到细胞。
The aim of this investigation was to determine whether luteal cells utilize cholesterol derived from high-density lipoprotein (HDL) for steroidogenesis and whether estrogen enhances luteal utilization of exogenous sterol. Incubation on day 15 corpora lutea (CL) with different doses of human HDL resulted in a dose-dependent increase in progesterone production. HDL in vitro enhanced the overall steroidogenic capacity. However, the percentage of increases in 17.alpha.-hydroxyprogesterone, testosterone and estradiol were significantly less than that of progesterone. Day 12 hypophysectomized and hysterectomized pregnant rats were treated with either estradiol, testosterone or vehicle for 72 h. Serum pregnenolone and progesterone were markedly increased by the steroid treatment, yet in vitro production of progesterone by CL in all the groups was similar. However, in the presence of HDL in the media, only luteal tissues from steroid-treated rats increased their progesterone outputs. The reduced production of progesterone by luteal cells of vehicle-treated rats was not due to an accumulation of pregnenolone but to an overall reduction in exogenous sterol utilization. Results suggest luteal cells of pregnant rats effectively utilize cholesterol from HDL from maximal steroidogenesis, and estradiol may stimulate luteal steroidogenesis, at least in part, by affecting the incorporation or utilization of cholesterol from HDL into the cell.