PDF(Pubmed)
Abstract：
The 1,2-dicarbonyl compound methylglyoxal (MGO) can react with and thereby impair the function of proteins and DNA, leading to pathophysiological pathways in vivo. However, studies on the bioavailability of dietary MGO and its reactions during digestion have diverging results. Therefore, simulated digestion experiments of MGO, protein, and creatine were performed in the dynamic, in vitro model of the upper gastrointestinal tract (TIM-1). This multicompartment model continuously adjusts pH values and has realistic gastrointestinal transit times while also removing water and metabolites by dialysis. Samples were analyzed with HPLC-UV for MGO and HPLC-MS/MS for creatine and glycated amino compounds. MGO reacted with creatine during simulated digestion in TIM-1 to form the hydroimidazolone MG-HCr in similar amounts as in a human intervention study. 28%-69% of MGO from the meal were passively absorbed in TIM-1, depending on the addition of creatine and protein. Simultaneous digestion of MGO with ovalbumin led to the formation of the lysine adduct N ε -carboxyethyllysine (CEL) and the methylglyoxal-derived hydroimidazolone of arginine (MG-H1). The formation of both compounds decreased with added creatine. Hence, glycation compounds are formed during digestion and significantly contribute to other ingested dietary glycation compounds, whose physiological consequences are critically discussed.
摘要：
1,2-二羰基化合物甲基乙二醛（MGO）可以与蛋白质和DNA反应，从而损害蛋白质和DNA的功能，导致体内病理生理途径。然而,关于膳食MGO的生物利用度及其在消化过程中的反应的研究结果不同。因此,MGO的模拟消化实验，蛋白质，肌酸是在动态中进行的，上消化道的体外模型(TIM-1)。这种多隔室模型连续调节pH值，并具有现实的胃肠道运输时间，同时还通过透析去除水和代谢物。用HPLC-UV分析样品的MGO和HPLC-MS/MS分析肌酸和糖化氨基化合物。MGO在TIM-1中模拟消化过程中与肌酸反应，形成与人类干预研究中相似量的氢咪唑酮MG-HCr。膳食中28%-69%的MGO在TIM-1中被动吸收,这取决于肌酸和蛋白质的添加。用卵清蛋白同时消化MGO导致赖氨酸加合物Nε-羧基乙基赖氨酸（CEL）和甲基乙二醛衍生的精氨酸氢咪唑酮（MG-H1）的形成。添加肌酸后，两种化合物的形成均减少。因此，糖化化合物在消化过程中形成，并显著促进其他摄入的饮食糖化化合物，其生理后果被严格讨论。
