Overproduction of VLDL1 driven by hyperglycemia is a dominant feature of diabetic dyslipidemia
Overproduction of VLDL1 driven by hyperglycemia is a dominant feature of diabetic dyslipidemia
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DOI：
10.1161/01.atv.0000172689.53992.25
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发表时间：
2005-08-01
影响因子：
8.7
通讯作者：
Taskinen, MR
中科院分区：
文献类型：
--
作者：
Adiels, M;Borén, J;Taskinen, MR
目的-我们试图比较VLDL 1和VLDL 2在2型糖尿病（DM 2）患者和非糖尿病受试者中的合成和代谢。方法和结果-我们使用一种新的多房室模型同时测定推注[H-2（3）]亮氨酸和[ H-2（5）]后VLDL 1和VLDL 2中载脂蛋白（apo）B和甘油三酯（TG）的动力学。甘油，并跟踪脂蛋白颗粒的催化和转移。我们的研究结果表明，在DM 2的VLDL颗粒的过量生产的解释是通过增强分泌的VLDL 1载脂蛋白B和TG。VLDL 2 apoB和TG的直接产生不受糖尿病本身的影响。VLDL 1 apoB和TG的产生速率密切相关，相应的池大小也是如此。VLDL 1和VLDL 2组成在DM 2和对照组中没有差异，并且新合成颗粒的TG与apoB比率在2组中非常相似。血浆葡萄糖，胰岛素，和游离脂肪酸一起解释了55%的变化，在VLDL 1 TG production rate.Conclusion -胰岛素抵抗和DM 2是与过量的肝脏生产的VLDL 1颗粒类似的大小和组成的非糖尿病受试者。我们认为，高血糖症是DM 2中VLDL 1过度产生的驱动力。
Objective - We sought to compare the synthesis and metabolism of VLDL1 and VLDL2 in patients with type 2 diabetes mellitus ( DM2) and nondiabetic subjects.Methods and Results - We used a novel multicompartmental model to simultaneously determine the kinetics of apolipoprotein ( apo) B and triglyceride ( TG) in VLDL1 and VLDL2 after a bolus injection of [H-2(3)] leucine and [ H-2(5)] glycerol and to follow the catabolism and transfer of the lipoprotein particles. Our results show that the overproduction of VLDL particles in DM2 is explained by enhanced secretion of VLDL1 apoB and TG. Direct production of VLDL2 apoB and TG was not influenced by diabetes per se. The production rates of VLDL1 apoB and TG were closely related, as were the corresponding pool sizes. VLDL1 and VLDL2 compositions did not differ in subjects with DM2 and controls, and the TG to apoB ratio of newly synthesized particles was very similar in the 2 groups. Plasma glucose, insulin, and free fatty acids together explained 55% of the variation in VLDL1 TG production rate.Conclusion - Insulin resistance and DM2 are associated with excess hepatic production of VLDL1 particles similar in size and composition to those in nondiabetic subjects. We propose that hyperglycemia is the driving force that aggravates overproduction of VLDL1 in DM2.