Prostaglandins suppress VLDL secretion in primary rat hepatocyte cultures: relationships to hepatic calcium metabolism.
Prostaglandins suppress VLDL secretion in primary rat hepatocyte cultures: relationships to hepatic calcium metabolism.
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发表时间：
1992-07
影响因子：
6.5
通讯作者：
Ó. Björnsson;J. Sparks;C. Sparks;G. Gibbons
中科院分区：
文献类型：
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作者：
Ó. Björnsson;J. Sparks;C. Sparks;G. Gibbons
在原代培养的大鼠肝细胞中，前列腺素E2和前列腺素D2(PGE2和PGD2)抑制极低密度脂蛋白(VLDL)相关载脂蛋白B、三酰甘油和胆固醇的分泌。这些影响是浓度依赖的，并且在至少3天的培养中仍然明显，对分泌的极低密度脂蛋白的载脂蛋白B/三酰甘油的比率没有影响。前列腺素对三酰甘油的总体合成没有影响，但三酰甘油在细胞内积累，而不是apoB在细胞内积累。与单独使用胰高血糖素相比，当PGE2与胰高血糖素一起加入到培养液中时，对VLDL分泌的抑制作用增强。但PGE2并不能增加胰升糖素对酮生成的刺激作用。与高血糖素不同，前列腺素既不抑制脂肪酸合成，也不刺激酮的生成或cAMP的产生。因此，在所有研究的肝脂代谢参数中，PGE2和PGD2选择性地影响极低密度脂蛋白。钙拮抗剂维拉帕米也选择性地抑制VLDL的分泌。二价阳离子载体A23187也抑制极低密度脂蛋白的释放，但相反，也抑制脂肪酸和胆固醇的合成。这些结果表明，极低密度脂蛋白的分泌是以某种最佳的细胞钙浓度来调节的，这可能是由前列腺素等药物选择性地介导的。
In primary cultures of rat hepatocytes, prostaglandin E2 and prostaglandin D2 (PGE2 and PGD2) inhibited the secretion of very low density lipoprotein (VLDL)-associated apoB, triacylglycerol, and cholesterol. These effects were concentration-dependent and remained apparent for at least 3 days of culture without an effect on the apoB/triacylglycerol ratio of the secreted VLDL. Prostaglandins had no effect on the overall synthesis of triacylglycerol but triacylglycerol accumulated within the cells, without intracellular accumulation of apoB. PGE2, when added to the medium together with glucagon, increased the inhibition of VLDL secretion, compared to that observed with glucagon alone. However, PGE2 did not increase the stimulatory effect of glucagon on ketogenesis. Unlike glucagon, the prostaglandins did not inhibit fatty acid synthesis nor did they stimulate ketogenesis or production of cAMP. Thus, of all the parameters of hepatic lipid metabolism studied, PGE2 and PGD2 selectively affected VLDL. Selective inhibition of VLDL secretion was also observed with the calcium antagonist verapamil. The divalent cation ionophore A23187 also inhibited VLDL release but, in contrast, also inhibited fatty acid and cholesterol synthesis. The results suggest that VLDL secretion is modulated at some optimal cell calcium concentration that may be mediated selectively by agents such as prostaglandins.