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首页> 外文期刊>Current opinion in lipidology >Lipif metabolism: insights into the complexity of VLDL metabolic pathways
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Lipif metabolism: insights into the complexity of VLDL metabolic pathways

机译：脂质代谢：深入了解VLDL代谢途径的复杂性

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The ability of liver to package lipids enriched in trigly-ceride with apoB to create VLDL particles for export to peripheral tissues is unique and complex. Recent publications have advanced our understanding of liver X receptors (LXR) and sterol-regulatory element-binding protein-1c (SREBP-1G) in regulation of lipogenesis and support a central role for insulin in VLDL biogenesis. Availability of a synthetic LXR ligand, T0901317, provides a strategy for studying LXR activation and downstream SREBP-1C-mediated effects. In studies by Oka-zaki et al., LXR activation in wild-type mice produced only mild and transient hypertriglyceridemia, which became dramatically increased in mice lacking LDL receptors, and this effect was prevented in mice lacking SREBP-1C. Under these conditions, phospholi-pid transfer protein (PLTP), which is activated both by LXR and SREBP-1G, becomes rate limiting in expanding the VLDL surface to accommodate additional core triglyceride. Enhanced production of chylomicron-sized particles was the result of an imbalance between the synergistic action of LXR and SREBP-1G on lipogenesis combined with enhanced transcription of PLTP and lack of clearance of triglyceride-rich lipoproteins by LDL receptors. Insulin may mediate direct effects on LXR transcript stability. T0901317 in hamsters enhanced SREBP-1G target gene expression, leading to induction of lipogenic genes and increased VLDL production without change in microsomal triglyceride transfer protein (MTP) mRNA and with a 30% reduction in apoB mRNA levels.
机译：肝脏用apoB包装富含甘油三酸酯的脂质产生VLDL颗粒以输出到周围组织的能力是独特而复杂的。最近的出版物已经使我们对肝脏X受体（LXR）和固醇调节元件结合蛋白1c（SREBP-1G）在脂肪形成的调节中的理解有了进一步的了解，并支持胰岛素在VLDL生物发生中的重要作用。合成LXR配体T0901317的可用性为研究LXR激活和下游SREBP-1C介导的作用提供了一种策略。在Oka-zaki等人的研究中，野生型小鼠中的LXR激活仅产生轻度和短暂的高甘油三酯血症，在缺乏LDL受体的小鼠中急剧升高，并且在缺乏SREBP-1C的小鼠中阻止了这种作用。在这些条件下，被LXR和SREBP-1G激活的磷脂-脂质转移蛋白（PLTP）在扩展VLDL表面以容纳额外的甘油三酸酯时成为速率限制。乳糜微粒大小颗粒产量的增加是LXR和SREBP-1G对脂肪生成的协同作用与PLTP转录增强以及LDL受体对富含甘油三酸酯的脂蛋白缺乏清除作用之间不平衡的结果。胰岛素可能介导对LXR转录物稳定性的直接影响。仓鼠中的T0901317增强了SREBP-1G靶基因的表达，从而导致脂肪基因的诱导和VLDL产量的增加，而微粒体甘油三酸酯转移蛋白（MTP）mRNA却没有变化，而apoB mRNA水平降低了30％。

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