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首页> 外文期刊>Current opinion in lipidology >Diabetic dyslipidaemia.
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Diabetic dyslipidaemia.

机译：糖尿病性血脂异常。

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PURPOSE OF REVIEW: Diabetic dyslipidaemia is a cluster of plasma lipid and lipoprotein abnormalities that are metabolically interrelated. The increase of large type 1 very low density lipoprotein particles in type 2 diabetes initiates a sequence of events that generates atherogenic remnants, small dense low-density lipoprotein and small dense high-density lipoprotein particles. Thus, it is of great importance to elucidate the mechanisms behind the overproduction of large very low density lipoprotein particles in diabetic dyslipidaemia. This review discusses the pathophysiology of very low density lipoprotein metabolism in type 2 diabetes and recent concepts of lipid management of diabetic dyslipidaemia. RECENT FINDINGS: Results indicate that triglyceride and apolipoprotein B production in types 1 and 2 very low density lipoprotein are significantly correlated, suggesting a coupling of the two processes governing the metabolism of these lipoprotein subpopulations. Insulin resistance, hyperglycaemia, andliver fat were associated with excess hepatic production of type 1 but not type 2 very low density lipoprotein particles. These data provide support for the independent regulation of types 1 and 2 very low density lipoprotein apolipoprotein B production. SUMMARY: Recent data suggest that the assembly of very low density lipoprotein is fundamentally altered in type 2 diabetes, explaining the overproduction of large type 1 very low density lipoprotein as well as the inability of insulin to suppress production of type 1 very low density lipoprotein in type 2 diabetes. Future discoveries hopefully will delineate the regulatory steps to allow more targeted treatment of diabetic dyslipidaemia.
机译：审查目的：糖尿病性血脂异常是一类血浆脂质和脂蛋白异常，与代谢相关。 2型糖尿病患者中1型超低密度脂蛋白大颗粒的增加引发一系列事件，这些事件会产生动脉粥样硬化残留物，小的，低密度的脂蛋白和小的，高密度的脂蛋白颗粒。因此，阐明糖尿病性血脂异常中超低密度脂蛋白大颗粒过量生产的背后机制非常重要。这篇综述讨论了2型糖尿病中极低密度脂蛋白代谢的病理生理以及糖尿病性血脂异常的脂质管理的最新概念。最近的发现：结果表明，在1型和2型极低密度脂蛋白中甘油三酸酯和载脂蛋白B的产生显着相关，表明控制这些脂蛋白亚群代谢的两个过程是相互关联的。胰岛素抵抗，高血糖症和肝脏脂肪与1型但非2型极低密度脂蛋白颗粒的过量肝产生有关。这些数据为1型和2型极低密度脂蛋白载脂蛋白B产生的独立调节提供了支持。摘要：最近的数据表明，在2型糖尿病中，极低密度脂蛋白的组装发生了根本性改变，从而解释了1型超低密度脂蛋白的生产过大以及胰岛素无法抑制1型极低密度脂蛋白的产生。 2型糖尿病。希望将来的发现将划定调控步骤，以使糖尿病性血脂异常的治疗更具针对性。

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