One hypothesis regarding the cause of diabetic complications is that advanced glycation end products (AGEs) bind to the AGE receptor and induce changes in gene expression. However, what AGEs exist in vivo and how individual AGEs are produced and impact body metabolic process to cause diabetes complications are not understood. We developed a new precise method to measure AGEs using LC-MS/MS with a new column and measured 7 free AGEs, including N(6)-carboxymethyllysine (CML), N(6)-(1-carboxyethyl)-l-lysine (CEL) and N5-(5-hydro-5-methyl-4-imidazolon-2-yl)L-ornithine (MG-H1), in human blood components. Blood was obtained from 9 people, and free AGEs were measured in individual blood components with LC-MS/MS before and after a meal. Free CML and CEL were abundant in erythrocytes, with 92% of free CML and 85% of free CEL localized in erythrocytes. In contrast, 60% of free MG-H1 was distributed in the serum. After the meal, free serum MG-H1 increased, but CML and CEL did not. CML and CEL are mainly distributed in erythrocytes and were not affected by the meal, indicating that they are produced in vivo. However, the main source of MG-H1 is the meal. The effect of genetic polymorphisms on AGEs was also investigated. Low activity type aldehyde dehydrogenase 2 (ALDH2) increased the CML concentration in the blood. This is the first observation that shows that the metabolic process of CML and CEL is different from that of MG-H1 and the effect of ALDH2 SNPs on CML.

关于糖尿病并发症的原因的一种假设是，晚期糖基化终末产物（AGEs）与AGE受体结合并诱导基因表达的变化。然而，尚不了解体内存在哪些AGEs，以及如何产生单个AGEs以及如何影响人体代谢过程以引起糖尿病并发症。我们开发了使用LC-MS / MS与新的列和测量7点免费的AGEs，包括N（6）-carboxymethyllysine（CML），N（6）来测量的AGEs新精确的方法- （1-羧基乙基） -升-赖氨酸（CEL）和N5-（5-氢-5-甲基-4-咪唑啉-2-基）L-鸟氨酸（MG-H1），在人的血液成分中。从9人那里采集血液，并在餐前和餐后用LC-MS / MS测定各个血液成分的游离AGEs。游离CML和CEL在红细胞中丰富，其中92％的游离CML和85％的游离CEL定位在红细胞中。相反，60％的游离MG-H1分布在血清中。饭后游离血清MG-H1增加，而CML和CEL则没有。CML和CEL主要分布在红细胞中，不受膳食影响，表明它们是体内产生的。但是，MG-H1的主要来源是膳食。还研究了遗传多态性对AGEs的影响。低活性醛脱氢酶2（ALDH2）可增加血液中的CML浓度。CML上的ALDH2 SNP。