Steinbrecher U P, Witztum J L
Diabetes. 1984 Feb;33(2):130-4. doi: 10.2337/diab.33.2.130.
In previous studies we have shown that extensive glucosylation of low-density lipoproteins (LDL) (40% of lysines modified) completely blocks receptor-mediated degradation in animals and in man. Other studies indicated that in some diabetics up to 5% of lysine residues of LDL were glucosylated. The present study was done to determine if the extent of glucosylation of LDL which can occur in diabetics could alter LDL catabolism. We measured degradation by cultured normal human fibroblasts and turnover in guinea pigs of various LDLs with 2-17% of lysine residues glucosylated. Modification of as few as 2-5% of lysines decreased LDL catabolism by 5-25%, and the degree of inhibition of catabolism was linearly related to the extent of LDL glucosylation. These results indicate that the extent of LDL glucosylation that can occur in diabetes may slow LDL catabolism and hence increase plasma LDL levels.
在先前的研究中，我们已经表明，低密度脂蛋白（LDL）的广泛糖基化（40%的赖氨酸被修饰）在动物和人类中完全阻断了受体介导的降解。其他研究表明，在一些糖尿病患者中，高达5%的LDL赖氨酸残基被糖基化。本研究旨在确定糖尿病患者中可能发生的LDL糖基化程度是否会改变LDL的分解代谢。我们测量了培养的正常人成纤维细胞对各种LDL的降解以及豚鼠体内LDL的周转情况，这些LDL的赖氨酸残基有2%-17%被糖基化。仅2%-5%的赖氨酸发生修饰就会使LDL分解代谢降低5%-25%，并且分解代谢的抑制程度与LDL糖基化程度呈线性相关。这些结果表明，糖尿病患者中可能发生的LDL糖基化程度可能会减缓LDL分解代谢，从而增加血浆LDL水平。
