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首页> 外文期刊>Journal of Lipid Research >ApoA-II expression in CETP transgenic mice increases VLDL production and impairs VLDL clearance.
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ApoA-II expression in CETP transgenic mice increases VLDL production and impairs VLDL clearance.

机译：CETP转基因小鼠中的ApoA-II表达会增加VLDL的产生并损害VLDL的清除。

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摘要

Apolipoprotein (apo)A-II is a major high density lipoprotein (HDL) protein; however, its role in lipoprotein metabolism is largely unknown. Transgenic (Tg) mice that overexpress human apoA-II present functional lecithin: cholesterol acyltransferase deficiency, HDL deficiency, hypertriglyceridemia and, when fed an atherogenic diet, increased non-HDL cholesterol and increased susceptibility to atherosclerosis. In contrast to humans, mice do not present cholesteryl ester transfer protein (CETP) activity in plasma. To study the in vivo interaction of these two proteins, we crossbred human apoA-II and CETP-Tg mice. CETP x apoA-II-Tg mice fed an atherogenic diet, compared with CETP-Tg mice presented a 2-fold decrease in HDL cholesterol and a quantitatively similar increase in total plasma cholesterol and percentage of free cholesterol, non-HDL cholesterol, and free fatty acids, together with a remarkable 112-fold increase in plasma triglycerides. Plasma triglycerides in CETP x apoA-II-Tg mice were mainly associated with very low density lipoproteins (VLDL), which were also enriched in protein content, and resulted from a combination of higher production rate compared with both of their progenitors and non-Tg control mice, and decreased catabolism compared only with CETP-Tg mice. These results show CETP x apoA-II-Tg mice to be a good model with which to study mechanisms leading to VLDL overproduction and suggest that CETP and, in particular apoA-II, may play a role in the regulation of VLDL metabolism.
机译：载脂蛋白（apo）A-II是主要的高密度脂蛋白（HDL）蛋白;然而，其在脂蛋白代谢中的作用尚不清楚。过度表达人类apoA-II的转基因（Tg）小鼠表现出功能性卵磷脂：胆固醇酰基转移酶缺乏症，HDL缺乏症，高甘油三酸酯血症，当进食有动脉粥样食物时，非HDL胆固醇增加，对动脉粥样硬化的敏感性增加。与人类相反，小鼠在血浆中不具有胆固醇酯转移蛋白（CETP）活性。为了研究这两种蛋白质的体内相互作用，我们将人类apoA-II和CETP-Tg小鼠杂交。与CETP-Tg小鼠相比，CETP x apoA-II-Tg小鼠进食了致动脉粥样化饮食，其HDL胆固醇降低了2倍，血浆总胆固醇和游离胆固醇，非HDL胆固醇和游离胆固醇的百分比在数量上相似。脂肪酸，以及血浆甘油三酸酯显着增加112倍。 CETP x apoA-II-Tg小鼠中的血浆甘油三酸酯主要与极低密度脂蛋白（VLDL）相关，后者还富含蛋白质含量，是由于与它们的祖细胞和非Tg相比生产率更高的结果对照小鼠，并且仅与CETP-Tg小鼠相比分解代谢降低。这些结果表明CETP x apoA-II-Tg小鼠是研究导致VLDL过量生产的机制的良好模型，并表明CETP，尤其是apoA-II，可能在VLDL代谢的调节中发挥作用。

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