A dose-response relationship between sex hormone-induced change in hepatic triglyceride lipase and high-density lipoprotein cholesterol in postmenopausal women.
A dose-response relationship between sex hormone-induced change in hepatic triglyceride lipase and high-density lipoprotein cholesterol in postmenopausal women.
复制标题
绝经后妇女性激素引起的肝甘油三酯脂肪酶和高密度脂蛋白胆固醇变化之间的剂量反应关系。
DOI：
10.1016/0026-0495(91)90129-k
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
Applebaum-Bowden,D
中科院分区：
文献类型：
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作者：
ColvinJr,PL;Auerbach,BJ;Case,LD;Hazzard,WR;Applebaum-Bowden,D
在以前的研究中，我们已经证明了肝素后肝甘油三酯脂肪酶（HTGL）对性类固醇的反应与高密度脂蛋白（HDL）胆固醇反应之间的时间关系。为了确定这种关系是否是剂量依赖性的，我们比较了两组六名绝经后妇女口服三种剂量的雌二醇和炔诺孕酮的效果。使用雌二醇后，肝素后HTGL活性从91 ± 46 nmol/min/mL降至50 ± 29 nmol/min/mL（基线至高剂量）（P<0.05）; HDL胆固醇从54 ± 6 mg/dL升高至64 ± 10 mg/dL（P<0.05）; HDL 2胆固醇从16 ± 4 mg/dL升高至23 ± 7 mg/dL（P<0.05）; HDL 3胆固醇浓度无变化。给予炔诺孕酮后，HTGL活性从79 ± 19增加到109 ± 24 nmol/min/mL（P< .05）; HDL胆固醇从64 ± 17降至43 ± 7 mg/dL HDL 2胆固醇从21 ± 17降至6 ± 5 mg/dL HDL 3胆固醇浓度从43 ± 8降至38 ± 8 mg/dL（P<0.05）。HTGL活性反应与雌激素剂量呈负相关（rs=-0.733，P = 0.0001），与孕酮剂量呈正相关（rs= 0.895，P = 0.0001）。HDL胆固醇反应与雌激素剂量直接相关（HDL：rs= 0.741，P = 0.001; HDL 2：rs= 0.586，P = 0.003），与孕酮剂量负相关（HDL：rs=-0.933，P = 0.0001; HDL 2：rs=-0.866，P = 0.0001; HDL 3：rs=-0.576，P = 0.003）。HDL胆固醇反应与两种性类固醇的HTGL反应呈负相关。口服性类固醇与HTGL和HDL反应之间的剂量-反应关系的证明为性类固醇诱导的HTGL活性变化可能导致观察到的HDL胆固醇浓度变化的假设提供了强有力的支持。
In previous studies, we have demonstrated a temporal relationship between the postheparin hepatic triglyceride lipase (HTGL) response to sex steroids and the high-density lipoprotein (HDL) cholesterol response. To determine if this relationship is dose-dependent, we compared the effect of three graduated doses of orally administered estradiol and norgestrel in two groups of six postmenopausal women. With estradiol administration, postheparin HTGL activity decreased from 91 ± 46 to 50 ± 29 nmol/min/mL, baseline to high dose (P< .05); HDL cholesterol increased from 54 ± 6 to 64 ± 10 mg/dL (P< .05); HDL2cholesterol increased from 16 ± 4 to 23 ± 7 mg/dL (P< .05); and HDL3cholesterol concentration did not change. With norgestrel administration, HTGL activity increased from 79 ± 19 to 109 ± 24 nmol/min/mL (P< .05); HDL cholesterol decreased from 64 ± 17 to 43 ± 7 mg/dL (P< .05); HDL2cholesterol decreased from 21 ± 17 to 6 ± 5 mg/dL (P< .05); and HDL3cholesterol concentration decreased from 43 ± 8 to 38 ± 8 mg/dL (P< .05). The HTGL activity response was inversely correlated with estrogen dose (rs= −.733,P= .0001) and directly correlated with progestin dose (rs= .895,P= .0001). The HDL cholesterol response was directly correlated with estrogen dose (HDL:rs= .741,P= .001; HDL2:rs= .586,P= 0.003) and inversely correlated with progestin dose (HDL:rs= −.933,P= .0001; HDL2:rs= −.866,P= .0001; HDL3:rs= −.576,P= .003). The HDL cholesterol response was inversely correlated with the HTGL response for both sex steroids. This demonstration of a dose-response relationship between orally administered sex steroids and the HTGL and HDL responses adds strong support to the hypothesis that the sex steroid-induced change in HTGL activity may cause the observed change in HDL cholesterol concentration.