Insulin suppression of VLDL apo B secretion is not mediated by the LDL receptor
Insulin suppression of VLDL apo B secretion is not mediated by the LDL receptor
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DOI：
10.1016/s0006-291x(02)02140-x
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发表时间：
2002-09-13
影响因子：
3.1
通讯作者：
Sparks, CE
中科院分区：
文献类型：
--
作者：
Chirieac, DV;Cianci, J;Sparks, CE
胰岛素抑制大鼠肝脏极低密度脂蛋白（VLDL）载脂蛋白B分泌。目前的研究通过检查胰岛素对来自Ldlr-/-和对照小鼠的肝细胞中VLDL apo B分泌的影响来测试胰岛素效应是否是LDL受体介导的。将原代肝细胞与含有C-14-亮氨酸和0.1 nM（基础）或200 nM胰岛素的培养基一起孵育过夜。然后，定量分泌的VLDL B100和B48。胰岛素降低了对照和Ldlr-/-肝细胞中C-14标记的B100和B48的水平，B 100降低了62 +/- 12% vs. 59 +/-12%，B48降低了56 +/- 11% vs. 61 +/- 9%。结果表明：（1）小鼠肝细胞通过减少VLDL apo B输出对胰岛素作出反应;（2）VLDL B 100和B48分泌均受到抑制;（3）胰岛素对VLDL apo B分泌的抑制作用在Ldlr-/-肝细胞中得以保留。(C)2002 Elsevier Science（美国）。All rights reserved.
Insulin inhibits hepatic very low density lipoprotein (VLDL) apo B secretion in rats. Current studies test whether the insulin effect is LDL receptor-mediated by examining the effect of insulin on VLDL apo B secretion in hepatocytes derived from Ldlr-/- and control mice. Primary hepatocytes were incubated overnight with media containing C-14-leucine and either 0.1 nM (basal) or 200 nM insulin. Afterwards, secreted VLDL B100 and B48 were quantitated. Insulin reduced C-14-labeled B100 and B48 comparably in control and Ldlr-/- hepatocytes with a 62 +/- 12% vs. 59 12% decrease in B 100, and a 56 +/- 11% vs. 61 +/- 9% decrease in B48. Results indicate: (1) mouse hepatocytes respond to insulin by reducing VLDL apo B output; (2) both VLDL B 100 and B48 secretion are suppressed; and (3) insulin inhibition of VLDL apo B secretion is retained in Ldlr-/- hepatocytes. (C) 2002 Elsevier Science (USA). All rights reserved.