INTESTINAL METABOLISM OF ESTROGENS
INTESTINAL METABOLISM OF ESTROGENS
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DOI：
10.1210/jcem-43-3-497
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发表时间：
1976-01-01
影响因子：
5.8
通讯作者：
TIKKANEN, MJ
中科院分区：
文献类型：
--
作者：
ADLERCREUTZ, H;MARTIN, F;TIKKANEN, MJ
用两种方法研究了雌激素在人肠道中的代谢。首先，在给药前和给药期间（2 g/d），测定12种雌激素在人类妊娠晚期粪便中的排泄情况。其次，给药5.4毫克和20毫克的16。对2例绝经后妇女口服羟孕酮，并在给药后0 ~ 150 min的时间间隔内同时抽取门脉和外周静脉血进行雌激素测定。正常妊娠粪便中的雌激素多数为未结合的。相对于主要雌激素雌三醇，雌二醇、雌酮和16-表雌三醇的排泄量大于妊娠胆汁、尿液和16- α。-羟孕酮，一种重要的胆道雌激素，只存在微量。大量的-羟基雌二醇。被发现。氨苄西林降低了肠道细菌类固醇代谢，导致结合雌激素的粪便排泄大量增加。它引起了非共轭和共轭雌三醇15 - α排泄的显著增加。-hydroxyestrone 15. alpha。-羟基雌二醇和2-甲氧基雌酮。这些发现强调了正常情况下肠道菌群对雌激素代谢的积极作用。注射16 α。-羟雄酮增加门静脉非共轭和共轭16 α。-hydroxyestrone, 16 - oxoestradiol - 17. - beta。15.α。-羟雌酮，16-表雌三醇和共轭雌三醇水平。两组患者中最显著的发现是门静脉未结合的15 - α -羟孕酮的大量增加。人类的肠道（或肠道内容物）可能有能力进行这种转化。-hydroxyestrone .fwdarw。15. alpha.-hydroxyestrone。外周血浆中也发现同样的雌激素增加，结合雌三醇的增加发生在外周血中，而在门脉血中发现。外周血浆值升高最大的是未偶联雌三醇和偶联16 α。-羟雄酮在接受20毫克剂量的受试者中未结合的16。-羟孕酮和16-雌二醇-17 - β在5.4毫克剂量的受试者中。雌激素的肠道和肠肝代谢也与这些发现有关。
Estrogen metabolism in the human intestine was studied in 2 ways. Firstly, by measuring the excretion of 12 estrogens in pooled human late pregnancy feces before and during the administration of ampicillin (2 g/day). Secondly, by administering 5.4 and 20 mg of 16.alpha.-hydroxyestrone orally to 2 postmenopausal women and analyzing the estrogens in simultaneously drawn portal and peripheral venous blood samples at time intervals from 0-150 min after steriod administraiton. The majority of the estrogens in normal pregnancy feces were unconjugated. The amounts of estradiol, estrone and 16-epiestriol excreted, relative to the principal estrogen estriol, were greater than in pregnancy bile or urine and 16.alpha.-hydroxyestrone, an important biliary estrogen, was only present in trace amounts. Considerable quantities of 15.alpha.-hydroxyestradiol-17.beta. were found. Ampicillin administration, which decreases intestinal bacterial steriod metabolism, caused a huge increase in the fecal excretion of conjugated estrogens. It caused very striking increases in the excretion of both unconjugated and conjugated, estriol, 15.alpha.-hydroxyestrone, 15.alpha.-hydroxyestradiol and 2-methoxyestrone. These findings emphasize the active role played by the intestinal microflora in estrogen metabolism under normal conditions. Administration of 16.alpha.-hydroxyestrone increased portal venous unconjugated and conjugated 16.alpha.-hydroxyestrone, 16-oxoestradiol-17.beta., 15.alpha.-hydroxyestrone, 16-epiestriol and conjugated estriol levels. The most significant finding in both subjects was the large increase in portal venous unconjugated 15.alpha.-hydroxyestrone. The human intestine (or intestinal contents) probably has the ability to carry out the transformation, 16.alpha.-hydroxyestrone .fwdarw. 15.alpha.-hydroxyestrone. Increases in the same estrogens were found in peripheral plasma, with the increase in conjugated estriol occurring in peripheral blood before it was seen in portal blood. The largest elevations in peripheral plasma values were seen in unconjugated estriol and conjugated 16.alpha.-hydroxyestrone in the subject who received the 20 mg dose and in unconjugated 16.alpha.-hydroxyestrone and 16-oxoestradiol-17.beta. in the subject who had the 5.4 mg dose. The intestinal and enterohepatic metabolsim of estrogens is discussed in relation to these findings.