Hayashi K, Koide K, Hirata Y, Ohtani H, Yamada K, Kajiyama G
Biochim Biophys Acta. 1986 Nov 14;879(2):140-8. doi: 10.1016/0005-2760(86)90096-2.
Cultured hepatocytes isolated from livers of 17 alpha-ethynylestradiol-treated rats were used to investigate the change of lipid metabolism induced by administration of 17 alpha-ethynylestradiol. Treatment with 17 alpha-ethynylestradiol caused a decrease of rat plasma lipids (free cholesterol, cholesterol ester, triacylglycerol and phosphatidylcholine). No difference in the ability of urea nitrogen synthesis could be demonstrated between cultured hepatocytes isolated from livers of 17 alpha-ethynylestradiol-treated rats and propylene glycol-treated rats (control). Total cholesterol and cholesterol ester contents of cultured hepatocytes isolated from livers of 17 alpha-ethynylestradiol-treated rats were increased in comparison with those of the control. Triacylglycerol content of cultured hepatocytes was not affected by 17 alpha-ethynylestradiol treatment. There was no difference in the composition of lipid content between liver tissues and cultured hepatocytes. These results suggest that hepatocytes isolated from livers maintain the character of livers treated with 17 alpha-ethynylestradiol or livers treated with propylene glycol. Free cholesterol and cholesterol ester synthesis from [14C]acetic acid by cultured hepatocytes isolated from livers of 17 alpha-ethynylestradiol-treated rats were decreased to about 30% of the control. Triacylglycerol and polar lipid (phospholipid) synthesis from [14C]acetic acid were not affected by 17 alpha-ethynylestradiol treatment. Microsomal hydroxymethylglutaryl-CoA reductase activity of rat liver treated with 17 alpha-ethynylestradiol was decreased to about 50% of control. The secretions of free cholesterol, cholesterol ester, triacylglycerol, phosphatidylcholine, apolipoprotein BL and BS by cultured hepatocytes isolated from livers of 17 alpha-ethynylestradiol treated rats were not decreased when compared with the control. Because lipid and apolipoprotein secretions from cultured hepatocytes treated with 17 alpha-ethynylestradiol were not decreased and cholesterol contents of liver tissues and cultured hepatocytes treated with 17 alpha-ethynylestradiol were increased and hepatic microsomal hydroxymethylglutaryl-CoA reductase activity was decreased by 17 alpha-ethynylestradiol treatment, it is suggested that the liver plays an important role in hypolipidemia induced by 17 alpha-ethynylestradiol by increasing the plasma lipid uptake mediated by an increased amount of lipoprotein receptors of liver membranes.
从经17α-乙炔雌二醇处理的大鼠肝脏中分离培养的肝细胞，用于研究给予17α-乙炔雌二醇后脂质代谢的变化。用17α-乙炔雌二醇处理导致大鼠血浆脂质（游离胆固醇、胆固醇酯、三酰甘油和磷脂酰胆碱）减少。在从经17α-乙炔雌二醇处理的大鼠肝脏和丙二醇处理的大鼠（对照）肝脏中分离培养的肝细胞之间，未发现尿素氮合成能力有差异。与对照相比，从经17α-乙炔雌二醇处理的大鼠肝脏中分离培养的肝细胞的总胆固醇和胆固醇酯含量增加。17α-乙炔雌二醇处理未影响培养肝细胞的三酰甘油含量。肝组织和培养肝细胞的脂质含量组成没有差异。这些结果表明，从肝脏分离的肝细胞保持了经17α-乙炔雌二醇处理或经丙二醇处理的肝脏的特征。从经17α-乙炔雌二醇处理的大鼠肝脏中分离培养的肝细胞由[14C]乙酸合成游离胆固醇和胆固醇酯的能力降至对照的约30%。17α-乙炔雌二醇处理未影响由[14C]乙酸合成三酰甘油和极性脂质（磷脂）的能力。经17α-乙炔雌二醇处理的大鼠肝脏微粒体羟甲基戊二酰辅酶A还原酶活性降至对照的约50%。与对照相比，从经17α-乙炔雌二醇处理的大鼠肝脏中分离培养的肝细胞分泌游离胆固醇、胆固醇酯、三酰甘油、磷脂酰胆碱、载脂蛋白BL和BS并未减少。由于经17α-乙炔雌二醇处理的培养肝细胞的脂质和载脂蛋白分泌未减少，且经17α-乙炔雌二醇处理的肝组织和培养肝细胞的胆固醇含量增加，以及17α-乙炔雌二醇处理使肝脏微粒体羟甲基戊二酰辅酶A还原酶活性降低，提示肝脏通过增加肝细胞膜脂蛋白受体数量介导的血浆脂质摄取，在17α-乙炔雌二醇诱导的低脂血症中起重要作用。
