Lopes-Virella M F, Sherer G, Wohltmann H, Sens D, Colwell J A
Metabolism. 1985 Dec;34(12):1079-85. doi: 10.1016/0026-0495(85)90150-7.
Low density lipoproteins (LDL) isolated from poorly controlled diabetic patients are known to be taken up and degraded by fibroblasts at a lower rate than LDL isolated from normal subjects. This aberrant metabolic behavior has been attributed to a diabetic-related abnormality in LDL composition yet to be characterized. The studies reported in this article show that the decrease in uptake and intracellular degradation of LDL from diabetic patients is further enhanced when the cells are exposed to lipoprotein deficient serum (LPDS) isolated from the same poorly controlled diabetic patients. Comparative studies of the composition of LPDS obtained from normal donors and poorly controlled diabetic patients showed an increase in saturated and total unesterified fatty acids (UFA), lecithin, apolipoprotein A1, and immunoreactive insulin in the LPDS from diabetic patients. We postulate that exposure of cells to LPDS obtained from poorly controlled diabetic patients may induce changes in the composition of the fibroblast membrane and alter its fluidity, leading to further decrease in the uptake and degradation of LDL. During poor diabetic control, cell membrane changes, and modification of LDL composition are likely to act either additively or synergistically to induce an abnormal LDL-cell interaction. This abnormal interaction may be a relevant factor to explain the greater incidence of arteriosclerosis in diabetes mellitus.
已知从控制不佳的糖尿病患者中分离出的低密度脂蛋白（LDL），其被成纤维细胞摄取和降解的速率低于从正常受试者中分离出的LDL。这种异常的代谢行为归因于LDL组成中与糖尿病相关的异常，但尚未明确其特征。本文报道的研究表明，当细胞暴露于从相同控制不佳的糖尿病患者中分离出的无脂蛋白血清（LPDS）时，糖尿病患者LDL摄取和细胞内降解的减少会进一步加剧。对从正常供体和控制不佳的糖尿病患者获得的LPDS组成的比较研究表明，糖尿病患者的LPDS中饱和脂肪酸和总未酯化脂肪酸（UFA）、卵磷脂、载脂蛋白A1和免疫反应性胰岛素增加。我们推测，细胞暴露于从控制不佳的糖尿病患者获得的LPDS可能会诱导成纤维细胞膜组成的变化并改变其流动性，导致LDL摄取和降解进一步减少。在糖尿病控制不佳期间，细胞膜变化和LDL组成的改变可能会以相加或协同的方式起作用，从而诱导异常的LDL-细胞相互作用。这种异常相互作用可能是解释糖尿病患者动脉粥样硬化发生率更高的一个相关因素。
