Non-enzymatic glycation (a.k.a. Maillard reaction) is a series of random spontaneous reactions between reducing sugars and amines, resulting in the formation of irreversible advanced glycation endproducts (AGE's). In food chemistry, this process is beneficial by contributing to the flavor, aroma, texture, and appearance of cooked foods. In vivo, however, Maillard reaction is deleterious because uncontrolled modification and crosslinking of biological macromolecules impairs their function. Consequently, chronic hyperglycemia of diabetes mellitus, for instance, leads to increased non-enzymatic glycation and diverse, multi-organ pathologies of diabetic complications. Based on the fact that toxic compounds, such as free radicals, are detoxified in vivo by specific defense mechanisms, one would expect to find mechanisms to control glucose toxicity as well. Thus far, only one such enzyme, fructosamine-3-kinase (FN3K), has been characterized. It operates intracellularly by catalyzing ATP-dependent removal of Maillard adducts, D-fructoselysines, from proteins, thereby reducing the Maillard reaction flux from glucose to AGE's. When FN3K was isolated, a closely related but distinct protein copurified with it. Unlike FN3K, however, this enzyme, fructosamine-3-kinase-related protein (FN3KRP), does not phosphorylate D-fructoselysines but it does phosphorylate several other (non-physiological) substrates. Interestingly, the distribution of FN3KRP in nature appears to be nearly universal whereas that of FN3K is limited to endotherms. In this article, it is suggested that the function of FN3KRP is deglycation of Maillard adducts downstream from fructoselysines. Such a mechanism, if proven correct, would be valuable given reports on apparent correlations between FN3KRP and some chronic conditions and/or diseases, such as a recent publication which proposes that the FN3KRP gene may be a longevity gene.

中文翻译：

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假设：果糖胺-3-激酶相关蛋白 (FN3KRP) 催化果糖胺直接下游的美拉德中间体的脱糖

非酶糖化（又名美拉德反应）是还原糖和胺之间的一系列随机自发反应，导致形成不可逆的晚期糖基化终产物 (AGE's)。在食品化学中，这一过程有助于改善熟食的风味、香气、质地和外观。然而，在体内，美拉德反应是有害的，因为生物大分子的不受控制的修饰和交联会损害它们的功能。因此，例如，糖尿病的慢性高血糖导致非酶糖化增加和糖尿病并发症的多种多器官病理。基于有毒化合物，如自由基，在体内解毒的事实通过特定的防御机制，人们还期望找到控制葡萄糖毒性的机制。迄今为止，只有一种这样的酶，果糖胺-3-激酶 (FN3K)，已被表征。它通过催化 ATP 依赖性从蛋白质中去除美拉德加合物 D-果糖赖氨酸而在细胞内起作用，从而减少从葡萄糖到 AGE 的美拉德反应通量。当分离出 FN3K 时，一种密切相关但不同的蛋白质与其共纯化。然而，与 FN3K 不同的是，这种酶，即果糖胺-3-激酶相关蛋白 (FN3KRP)，不会磷酸化 D-果糖赖氨酸，但会磷酸化其他几种（非生理）底物。有趣的是，FN3KRP 在自然界的分布似乎几乎是普遍的，而 FN3K 的分布仅限于吸热。在本文中，建议 FN3KRP 的功能是果糖赖氨酸下游美拉德加合物的脱糖。考虑到 FN3KRP 与某些慢性病和/或疾病之间的明显相关性的报告，如最近发表的文章提出 FN3KRP 基因可能是长寿基因，这种机制如果被证明是正确的，将是有价值的。