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首页> 外文期刊>Life sciences >Circulating advanced glycation peptides in streptozotocin-induced diabetic rats: evidence for preferential modification of IgG light chains.
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Circulating advanced glycation peptides in streptozotocin-induced diabetic rats: evidence for preferential modification of IgG light chains.

机译：链脲佐菌素诱导的糖尿病大鼠中循环高级糖基化肽：IgG轻链优先修饰的证据。

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As the glycation/glycoxidation hypothesis for the genesis of diabetic complications is achieving widespread acceptance, much attention is being paid to the role of low molecular weight advanced glycation (AGE) adducts, as second generation glycating agents. We set out a study with the objective of attesting the presence of increased amounts of AGE-peptides in the circulation of streptozotocin-induced diabetic rats and to determine the nature of the plasma proteins which are main targets for advanced glycation. AGE (Ex 370/Em 440 nm) and pentosidine fluorescence (Ex 335/Em 385 nm) were significantly higher in plasma from diabetic rats after only one month of hyperglycemia as compared to controls (35 +/- 7 vs 25 +/- 2 AU, p< 0.05 and 54 +/- 14 vs 27 +/- 3 AU, p< 0.01 respectively). AGE-peptides (<10 kDa) were more than two-fold higher in diabetic animals. Immunoblots after SDS-PAGE of plasma proteins showed that AGE-IgG displayed a selective predominant increment in the same animals. When native rat IgG was incubated in the presence of AGE-peptides isolated from diabetic animals, AGE modification was already apparent after only 24 h of incubation, and was particularly important for light chains. AGE-immunoreactive light chains displayed an apparent increase in molecular weight. Aminoguanidine prevented, while copper enhanced AGE binding to IgG light chains. Our data validate the streptozotocin-induced diabetic rat as a model reproducing the presence of circulating AGE-peptides, give evidence that IgG are preferential targets for advanced glycation in plasma and suggest that this modification, mediated by AGE-peptides, can be prevented by aminoguanidine.
机译：随着糖尿病并发症起源的糖化/糖氧化假设得到了广泛的接受，作为第二代糖化剂的低分子量高级糖化（AGE）加合物的作用已引起人们的广泛关注。我们进行了一项研究，目的是证明在链脲佐菌素诱导的糖尿病大鼠的循环中存在数量增加的AGE肽，并确定血浆蛋白的性质，血浆蛋白是晚期糖基化的主要靶标。仅高血糖一个月后，糖尿病大鼠血浆中的AGE（Ex 370 / Em 440 nm）和戊糖苷荧光（Ex 335 / Em 385 nm）与对照组相比显着更高（35 +/- 7 vs 25 +/- 2 AU，p <0.05和54 +/- 14与27 +/- 3 AU，p <0.01）。在糖尿病动物中，AGE肽（<10 kDa）高出两倍以上。对血浆蛋白进行SDS-PAGE后的免疫印迹表明，AGE-IgG在同一动物中显示出选择性的主要增量。当在从糖尿病动物分离的AGE肽存在下孵育天然大鼠IgG时，仅在孵育24小时后AGE修饰就已经很明显，并且对轻链尤为重要。 AGE-免疫反应性轻链显示出分子量的明显增加。氨基胍可预防，而铜可增强AGE与IgG轻链的结合。我们的数据验证了链脲佐菌素诱导的糖尿病大鼠为可复制循环AGE肽存在的模型，证明IgG是血浆中晚期糖基化的优先靶标，并表明由AGE肽介导的这种修饰可被氨基胍阻止。

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