关键词: allulose fructose glucose glycation

Mesh : Animals Glycation End Products, Advanced / metabolism Rats Glycosylation Fructose / metabolism Monosaccharides / metabolism Glucose / metabolism Male Serum Albumin, Bovine / metabolism Receptor for Advanced Glycation End Products / metabolism Rats, Sprague-Dawley

来  源:   DOI:10.3390/ijms25136921   PDF(Pubmed)

Abstract:
A complication of reducing sugars is that they can undergo Maillard chemical reactions, forming advanced glycation end-products (AGEs) that can induce oxidative stress and inflammation via engagements with the main receptor for AGEs (RAGE) in various tissues. Certain sugars, such as glucose and fructose, are well known to cause AGE formation. Recently, allulose has emerged as a rare natural sugar that is an epimer of fructose and which is of low caloric content that is minimally metabolized, leading to it being introduced as a low-calorie sugar alternative. However, the relative ability of allulose to generate AGEs compared to glucose and fructose is not known. Here we assess the accumulation of AGEs in cell-free, in vitro, and in vivo conditions in response to allulose and compare it to glycation mediated by glucose or fructose. AGEs were quantified in cell-free samples, cell culture media and lysates, and rat serum with glycation-specific ELISAs. In cell-free conditions, we observed concentration and time-dependent increases in AGEs when bovine serum albumin (BSA) was incubated with glucose or fructose and significantly less glycation when incubated with allulose. AGEs were significantly elevated when pulmonary alveolar type II-like cells were co-incubated with glucose or fructose; however, significantly less AGEs were detected when cells were exposed to allulose. AGE quantification in serum obtained from rats fed a high-fat, low-carb (HFLC) Western diet for 2 weeks revealed significantly less glycation in animals co-administered allulose compared to those exposed to stevia. These results suggest allulose is associated with less AGE formation compared to fructose or glucose, and support its safety as a low-calorie sugar alternative.
摘要:
还原糖的一个复杂因素是它们可以经历美拉德化学反应,形成晚期糖基化终产物(AGEs),可通过与各种组织中AGEs的主要受体(RAGE)的参与诱导氧化应激和炎症。某些糖,比如葡萄糖和果糖,众所周知,它能导致AGE的形成。最近,阿洛酮糖已经成为一种罕见的天然糖,它是果糖的差向异构体,热量含量低,代谢最少,导致它被引入作为低热量的糖替代品。然而,与葡萄糖和果糖相比,阿洛酮糖产生AGEs的相对能力尚不清楚。在这里,我们评估了无细胞中AGEs的积累,在体外,和体内条件对阿洛酮糖的反应,并将其与葡萄糖或果糖介导的糖化进行比较。在无细胞样品中定量AGEs,细胞培养基和裂解物,和具有糖基化特异性ELISA的大鼠血清。在无细胞条件下,我们观察到,当牛血清白蛋白(BSA)与葡萄糖或果糖孵育时,AGEs的浓度和时间依赖性增加,当与阿洛酮糖孵育时,糖基化显著减少.当肺泡II型细胞与葡萄糖或果糖共孵育时,AGEs显着升高;然而,当细胞暴露于阿洛酮糖时,检测到的AGEs显著减少.从高脂肪喂养的大鼠获得的血清中的AGE定量,低碳水化合物(HFLC)西方饮食2周显示,与暴露于甜叶菊的动物相比,共同施用阿洛酮糖的动物的糖化明显减少。这些结果表明,与果糖或葡萄糖相比,阿洛酮糖与更少的AGE形成有关。并支持其作为低热量糖替代品的安全性。
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