Witztum J L, Steinbrecher U P, Kesaniemi Y A, Fisher M
Proc Natl Acad Sci U S A. 1984 May;81(10):3204-8. doi: 10.1073/pnas.81.10.3204.
Nonenzymatic glucosylation interferes with recognition of low density lipoprotein (LDL) by its receptor and markedly decreases the rate of plasma clearance of glucosylated LDL, both in experimental animals and in normal human subjects. However, in selected diabetic subjects we have observed a paradoxical increase in the clearance of glucosylated LDL, suggesting the possibility of immune-mediated clearance. Immunoassay demonstrated antibodies specific for glucosylated LDL in the preinjection plasma of each of four such diabetic subjects studied. These antibodies cross-react with other glucosylated proteins and recognize specifically the glucosylated lysine epitope--i.e., glucitollysine . These data suggest that nonenzymatic glucosylation of plasma or structural proteins may render them immunogenic and result in production of autoantibodies that recognize not only the particular immunogen but also many other glucosylated proteins, including glucosylated tissue proteins. These findings may be relevant to the increased prevalence of immune complexes in plasma of diabetic subjects and the late complications of diabetes mellitus.
非酶糖基化会干扰低密度脂蛋白(LDL)与其受体的识别,并显著降低实验动物和正常人类受试者体内糖基化LDL的血浆清除率。然而,在部分糖尿病患者中,我们观察到糖基化LDL的清除率出现了反常的升高,提示存在免疫介导清除的可能性。免疫分析显示,在所研究的4名此类糖尿病患者的注射前血浆中,均存在针对糖基化LDL的特异性抗体。这些抗体可与其他糖基化蛋白发生交叉反应,并特异性识别糖基化赖氨酸表位,即葡糖胺赖氨酸。这些数据表明,血浆或结构蛋白的非酶糖基化可能使其具有免疫原性,并导致产生不仅能识别特定免疫原,还能识别许多其他糖基化蛋白(包括糖基化组织蛋白)的自身抗体。这些发现可能与糖尿病患者血浆中免疫复合物患病率的增加以及糖尿病的晚期并发症有关。