Sanfirova V M, Titov V N, Gromadova M
Vopr Med Khim. 1987 Mar-Apr;33(2):77-83.
Effect of estradiol ethynyl and estradiol propionate on esterification of saturated and non-saturated fatty acids in liver tissue, as one of possible mechanisms in development of estrogen-induced hypertriglyceridemia, was studied using labelled precursors 3H-palmitic and 14C-linoleic acids. Both these estrogens stimulated the incorporation of exogenous fatty acids into triglycerides. After administration of estradiol dipropionate relative esterification of 14C-linoleic acid into triglycerides was increased as compared with controls. Estradiol ethynyl increased and estradiol dipropionate decreased the incorporation of exogenous fatty acids into liver phospholipids. Both estrogens activated the relative esterification of linoleic acid into phospholipids. A decrease in exogenous fatty acids esterification into fraction of cholesterol esters, caused by both these estrogens, occurred due to an increase in relative incorporation of linoleic acid into these lipids. As shown in experiments of relative esterification of saturated and non-saturated fatty acids, estradiol propionate stimulated synthesis of more non-saturated forms of triglycerides, phospholipids and cholesterol esters in rat liver tissue as compared with the estradiol ethynyl action. The data obtained and the data of literature suggest that activation of exogenous fatty acids esterification into triglycerides and alterations in relative esterification of saturated and non-saturated fatty acids into triglycerides and phospholipids of liver tissue are of importance in pathogenesis of estrogen-induced hypertriglyceridemia.
使用标记前体3H-棕榈酸和14C-亚油酸,研究了乙炔雌二醇和丙酸雌二醇对肝组织中饱和与不饱和脂肪酸酯化的影响,这是雌激素诱导的高甘油三酯血症发生的可能机制之一。这两种雌激素均刺激外源性脂肪酸掺入甘油三酯。与对照组相比,给予二丙酸雌二醇后,14C-亚油酸相对酯化到甘油三酯中的量增加。乙炔雌二醇增加而二丙酸雌二醇减少外源性脂肪酸掺入肝磷脂。两种雌激素均激活亚油酸相对酯化到磷脂中。这两种雌激素导致外源性脂肪酸酯化到胆固醇酯部分减少,这是由于亚油酸相对掺入这些脂质增加所致。如饱和与不饱和脂肪酸相对酯化实验所示,与乙炔雌二醇的作用相比,丙酸雌二醇刺激大鼠肝组织中甘油三酯、磷脂和胆固醇酯的更多不饱和形式的合成。获得的数据和文献数据表明,外源性脂肪酸酯化到甘油三酯的激活以及饱和与不饱和脂肪酸相对酯化到肝组织甘油三酯和磷脂中的改变在雌激素诱导的高甘油三酯血症的发病机制中具有重要意义。