Circulating low -molecular weight AGEs in the development and progression of diabetic complications

糖尿病患者体内的高水平糖会导致许多器官受损，包括心脏、眼睛和肾脏。这些高糖通过多种机制引起损伤，其中之一是通过蛋白质和葡萄糖之间的不可逆反应形成晚期糖基化终产物或AGEs。这种反应导致AGE修饰分子的形状和功能发生变化，从而逐渐导致器官损伤。AGEs还结合并激活促进组织损伤和瘢痕形成的特异性受体。在葡萄糖浓度高的地方，AGEs积累得更快。这就是为什么血糖控制良好的患者比那些无法控制血糖的患者做得更好的原因之一。阻断AGEs的形成能够防止糖尿病动物的肾脏损伤，这一事实说明了AGE通路的重要性。此外，在没有高糖的情况下，暴露于AGEs可导致糖尿病样变化。我们的实验室在研究晚期糖基化和阻断这一过程的方法方面处于世界领先地位。该研究将调查实验动物和糖尿病患者的AGEs循环水平，并将其与糖尿病并发症的发生和进展相关联

High levels of sugars seen in patients with diabetes leads to damage of many organs including the heart, the eyes and the kidneys. These high sugars cause damage through a number of mechanisms, one being the formation of advanced glycation end products or AGEs, formed by the irreversible reaction between proteins and glucose. This reaction leads to a change in the shape and function of AGE-modified molecules that progressively contributes to organ damage. AGEs also bind and activate specific receptors that promote the damage and scarring of tissue. Where the glucose concentration is high, AGEs accumulate much more quickly. This is one reason why patients with good sugar control do better than those who are unable to control their blood sugars. The importance of this AGE pathway is illustrated by the fact that blocking the formation of AGEs is able to prevent kidney damage in animals with diabetes. In addition, exposure to AGEs can cause diabetes-like changes in the absence of high sugars. Our laboratory is a world leader in the study of the advanced glycation and methods blocking this process. The research proposed will investigate circulating levels of AGEs in experimental animals and patients with diabetes, and correlate them with the development and progression of complications of diabetes