Szafran H, Smielak-Korombel W
Oddziału Kardiologii Wojewódzkiego, Szpitala Specjalistycznego, im. G. Narutowicza w Krakowie.
Przegl Lek. 1998;55(5):266-70.
In the view of lipid metabolism, adipose tissue and liver are the most important tissues for 17-beta-estradiol, the main estrogen in women's body. The lack of estrogens in women after menopause may cause coronary heart disease. It is considered, that 25 to 50% of positive effect of estrogens which are given to postmenopausal women is connected with their action on lipid metabolism. Blood plasma parameters which characterize lipid metabolism return to their physiological values during estrogens therapy. Estrogens are transferred to adipose tissue cells and liver cells by endocrine and paracrine way. They are also produced in these cells from androgens. In adipocytes 17-beta-estradiol can be stored as its esters with long-chain fatty acids. It was proved that estrogens receptors are present in adipocytes and hepatocytes but their density is much lower than in gonads. On the cellular level estrogens regulate mRNA production for particular proteins among which there are proteins involved in lipid metabolism. In adipose tissue 17-beta-estradiol has a direct effect on lipoprotein lipase (LPL) and hormone-sensitive lipase (HSL). In the case of the first enzyme its synthesis is faster, while the synthesis of the latter is slower. On the other hand, indirect action of estrogens on adipose tissue is connected with the stimulation of the releasing of other hormones which increase HSL activity. To this group of hormones there belong catecholamines, growth hormone (GH) and glucagon. In liver 17-beta-estradiol regulates the rate of synthesis of structural apolipoproteins for VLDL and HDL. 17-beta-estradiol reduces the rate of apoB-100 synthesis, while stimulates apoA-I and apoA-II synthesis. HDL fraction containing apoA-I and apoA-II is necessary for chylomicrons and VLDL degradation as well as direct and indirect cholesterol transport to liver. Moreover, in hepatocytes estrogens stimulate the synthesis of apoC-III, while they decrease the synthesis of hepatic lipase (HL). In conclusion, 17-beta-estradiol by regulating lipid metabolism in adipocytes and hepatocytes modulates the concentration of lipid substances in plasma. The lack of 17-beta-estradiol leads likely to various lipid metabolism disorders in women after menopause. Estrogens therapy in these postmenopausal women may result in the improvement of lipid metabolism.
从脂质代谢的角度来看，脂肪组织和肝脏是女性体内主要雌激素17-β-雌二醇作用的最重要组织。绝经后女性体内雌激素缺乏可能会引发冠心病。据认为，给予绝经后女性的雌激素有25%至50%的积极作用与其对脂质代谢的作用有关。在雌激素治疗期间，表征脂质代谢的血浆参数会恢复到生理值。雌激素通过内分泌和旁分泌方式转移到脂肪组织细胞和肝细胞中。它们也在这些细胞中由雄激素产生。在脂肪细胞中，17-β-雌二醇可以与其长链脂肪酸酯一起储存。已证明雌激素受体存在于脂肪细胞和肝细胞中，但其密度远低于性腺中的密度。在细胞水平上，雌激素调节特定蛋白质的mRNA产生，其中包括参与脂质代谢的蛋白质。在脂肪组织中，17-β-雌二醇对脂蛋白脂肪酶（LPL）和激素敏感性脂肪酶（HSL）有直接作用。对于第一种酶，其合成更快，而后者的合成较慢。另一方面，雌激素对脂肪组织的间接作用与刺激增加HSL活性的其他激素的释放有关。这一类激素包括儿茶酚胺、生长激素（GH）和胰高血糖素。在肝脏中，17-β-雌二醇调节极低密度脂蛋白（VLDL）和高密度脂蛋白（HDL）结构载脂蛋白的合成速率。17-β-雌二醇降低载脂蛋白B-100的合成速率，同时刺激载脂蛋白A-I和载脂蛋白A-II的合成。含有载脂蛋白A-I和载脂蛋白A-II的HDL部分对于乳糜微粒和VLDL的降解以及胆固醇向肝脏的直接和间接转运是必需的。此外，在肝细胞中，雌激素刺激载脂蛋白C-III的合成，同时降低肝脂肪酶（HL）的合成。总之，17-β-雌二醇通过调节脂肪细胞和肝细胞中的脂质代谢来调节血浆中脂质物质的浓度。17-β-雌二醇的缺乏可能导致绝经后女性出现各种脂质代谢紊乱。对这些绝经后女性进行雌激素治疗可能会改善脂质代谢。
