ACCUMULATION OF MAILLARD REACTION-PRODUCTS IN SKIN COLLAGEN IN DIABETES AND AGING
ACCUMULATION OF MAILLARD REACTION-PRODUCTS IN SKIN COLLAGEN IN DIABETES AND AGING
复制标题
DOI：
10.1172/jci116481
复制
发表时间：
1993-06-01
影响因子：
15.9
通讯作者：
BAYNES, JW
中科院分区：
文献类型：
--
作者：
DYER, DG;DUNN, JA;BAYNES, JW
为了研究糖化和氧化反应对衰老和糖尿病中不溶性胶原蛋白修饰的贡献，测定了39例1型糖尿病患者和52例非糖尿病对照者皮肤胶原蛋白中的美拉德反应产物。研究的化合物包括果糖赖氨酸（FL），最初的糖化产物，和糖氧化产物，N（N）-（羧甲基）赖氨酸（CML）和戊糖苷，形成在后来的美拉德反应。还研究了胶原连接的荧光。在非糖尿病受试者中，胶原蛋白的糖化（FL含量）在20至85岁之间仅增加33%。与此相反，慢性粒细胞白血病，戊糖苷和荧光增加五倍，与年龄密切相关。在糖尿病患者中，胶原FL增加3倍，与非糖尿病受试者相比，强烈相关的糖化血红蛋白，但不与年龄。与对照组患者相比，糖尿病患者的CML胶原蛋白、戊糖苷和荧光增加了两倍：这可以通过单独的糖化增加来解释，而不引起氧化应激增加。在两组中，CML、戊糖苷和荧光之间存在很强的相关性，这为通过美拉德反应对胶原进行年龄依赖性化学修饰以及糖尿病中该过程的加速提供了证据。这些结果支持了糖尿病作为一种疾病的描述，其特征是长寿命组织蛋白的加速化学老化。
To investigate the contribution of glycation and oxidation reactions to the modification of insoluble collagen in aging and diabetes, Maillard reaction products were measured in skin collagen from 39 type 1 diabetic patients and 52 nondiabetic control subjects. Compounds studied included fructoselysine (FL), the initial glycation product, and the glycoxidation products, N(epsilon)-(carboxymethyl)lysine (CML) and pentosidine, formed during later Maillard reactions. Collagen-linked fluorescence was also studied. In nondiabetic subjects, glycation of collagen (FL content) increased only 33% between 20 and 85 yr of age. In contrast, CML, pentosidine and fluorescence increased five-fold, correlating strongly with age. In diabetic patients, collagen FL was increased threefold compared with nondiabetic subjects, correlating strongly with glycated hemoglobin but not with age. Collagen CML, pentosidine and fluorescence were increased up to twofold in diabetic compared with control patients: this could be explained by the increase in glycation alone, without invoking increased oxidative stress. There were strong correlations among CML, pentosidine and fluorescence in both groups, providing evidence for age-dependent chemical modification of collagen via the Maillard reaction, and acceleration of this process in diabetes. These results support the description of diabetes as a disease characterized by accelerated chemical aging of long-lived tissue proteins.