Adiels Martin, Taskinen Marja-Riitta, Borén Jan
Wallenberglaboratoriet, Bruna Stråket 16, Sahlgrenska University Hospital, 41345 Göteborg, Sweden.
Curr Diab Rep. 2008 Feb;8(1):60-4. doi: 10.1007/s11892-008-0011-4.
After recently being recognized as a feature of the metabolic syndrome, fatty liver has evolved as a key player in the pathogenesis of dyslipidemia. Development of nonalcoholic fatty liver disease comes from an imbalance between the influx and production of fatty acids and the use of fatty acids for oxidation or secretion as very low density lipoprotein (VLDL) triglycerides. Previously, we have shown a strong relationship between increased liver fat and overproduction of large VLDL particles. We observed recently that in patients with high liver fat, insulin was unable to regulate VLDL production. The result is increased concentrations of VLDL particles in the circulation. Consequently, changes are seen in the metabolism of other lipoproteins that interact with VLDL particles, the net result being decreased high-density lipoprotein cholesterol and increased formation of small, dense low-density lipoprotein. In this article, we review recent findings on the development of fatty liver and its role in the diabetic dyslipidemia pathogenesis.
在最近被认定为代谢综合征的一项特征后，脂肪肝已成为血脂异常发病机制中的关键因素。非酒精性脂肪性肝病的发展源于脂肪酸流入与生成之间的失衡，以及脂肪酸用于氧化或作为极低密度脂蛋白（VLDL）甘油三酯分泌的过程。此前，我们已表明肝脏脂肪增加与大型VLDL颗粒的过度生成之间存在密切关系。我们最近观察到，在肝脏脂肪含量高的患者中，胰岛素无法调节VLDL的生成。结果是循环中VLDL颗粒的浓度增加。因此，与VLDL颗粒相互作用的其他脂蛋白的代谢出现变化，最终结果是高密度脂蛋白胆固醇降低，小而密的低密度脂蛋白形成增加。在本文中，我们综述了关于脂肪肝发展及其在糖尿病血脂异常发病机制中作用的最新研究发现。
