女性为何比男性寿命更长：长寿中性别差异的生物学机制。

Why women live longer than men: the biologic mechanism of the sex differential in longevity.

Hazzard W R, Applebaum-Bowden D

Department of Internal Medicine, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, NC.

Trans Am Clin Climatol Assoc. 1990;101:168-88; discussion 188-9.

Exogenous sex steroids appear to influence lipoproteins in a manner that is a caricature of the effects of endogenous sex steroids: Estrogens raise HDL (selectively HDL2) and lower LDL; Androgens lower HDL (selectively HDL2), while raising LDL. 2. Exogenous sex steroids are likely to affect LDL metabolism via effects on the LDL receptor; Estrogens increase LDL receptor activity (in non-human species at both the hepatic cellular and mRNA levels, though this is yet to be confirmed in humans); ??Androgens decrease LDL receptor activity (yet to be tested in either human or non-human species). 3. Exogenous sex steroids appear to alter HDL levels predominantly via modulation of HDL catabolism; Estrogens retard HDL catabolism (33) (and may also increase apo A-I synthesis and HDL production); Androgens accelerate HDL catabolism (30). 4. Modulation of HDL (and possibly LDL) metabolism by sex steroids may be mediated by alterations in hepatic triglyceride lipase (HTGL) activity.

外源性性类固醇似乎以一种类似于内源性性类固醇作用的方式影响脂蛋白：雌激素升高高密度脂蛋白（选择性地升高高密度脂蛋白2）并降低低密度脂蛋白；雄激素降低高密度脂蛋白（选择性地降低高密度脂蛋白2），同时升高低密度脂蛋白。2. 外源性性类固醇可能通过对低密度脂蛋白受体的作用来影响低密度脂蛋白代谢；雌激素增加低密度脂蛋白受体活性（在非人类物种中，在肝细胞水平和mRNA水平均有增加，不过这一点在人类中尚未得到证实）；雄激素降低低密度脂蛋白受体活性（在人类或非人类物种中均有待测试）。3. 外源性性类固醇似乎主要通过调节高密度脂蛋白分解代谢来改变高密度脂蛋白水平；雌激素延缓高密度脂蛋白分解代谢（33）（并且可能还会增加载脂蛋白A-I合成和高密度脂蛋白生成）；雄激素加速高密度脂蛋白分解代谢（30）。4. 性类固醇对高密度脂蛋白（可能还有低密度脂蛋白）代谢的调节可能是通过肝甘油三酯脂肪酶（HTGL）活性的改变来介导的。

Why women live longer than men: the biologic mechanism of the sex differential in longevity.