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不同单糖暴露后糖化的差异速率。

Differential Rates of Glycation Following Exposure to Unique Monosaccharides.

机构信息

Department of Cell Biology and Physiology, Brigham Young University, Provo, UT 84602, USA.

Sansum Diabetes Research Institute, Santa Barbara, CA 93105, USA.

出版信息

Int J Mol Sci. 2024 Jun 25;25(13):6921. doi: 10.3390/ijms25136921.

DOI:10.3390/ijms25136921
PMID:39000037
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11240907/
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

还原糖的一个并发症是,它们可以进行美拉德化学反应,形成高级糖基化终产物(AGEs),通过与各种组织中 AGEs 的主要受体(RAGE)结合,诱导氧化应激和炎症。某些糖,如葡萄糖和果糖,众所周知会导致 AGE 的形成。最近,阿洛酮糖作为一种罕见的天然糖脱颖而出,它是果糖的差向异构体,热量低,代谢极少,因此被引入作为低热量糖替代品。然而,阿洛酮糖与葡萄糖和果糖相比生成 AGE 的相对能力尚不清楚。在这里,我们评估了在无细胞、体外和体内条件下,阿洛酮糖对 AGE 积累的反应,并将其与葡萄糖或果糖介导的糖化进行了比较。使用糖化特异性 ELISA 在无细胞样品、细胞培养物培养基和裂解物以及大鼠血清中定量 AGEs。在无细胞条件下,当牛血清白蛋白(BSA)与葡萄糖或果糖孵育时,我们观察到 AGEs 的浓度和时间依赖性增加,而与阿洛酮糖孵育时则显著减少糖化。当肺泡 II 型样细胞与葡萄糖或果糖共孵育时,AGEs 显著升高;然而,当细胞暴露于阿洛酮糖时,检测到的 AGEs 明显减少。从喂食高脂肪、低碳水化合物(HFLC)西方饮食 2 周的大鼠获得的血清中进行 AGE 定量,结果显示与单独摄入甜菊糖相比,同时给予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,阿洛酮糖与较少的 AGE 形成有关,并支持其作为低热量糖替代品的安全性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/694d/11240907/6675f68ea675/ijms-25-06921-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/694d/11240907/386336ae598b/ijms-25-06921-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/694d/11240907/4b6eb55cfef1/ijms-25-06921-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/694d/11240907/e093014b59ae/ijms-25-06921-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/694d/11240907/6675f68ea675/ijms-25-06921-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/694d/11240907/386336ae598b/ijms-25-06921-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/694d/11240907/4b6eb55cfef1/ijms-25-06921-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/694d/11240907/e093014b59ae/ijms-25-06921-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/694d/11240907/6675f68ea675/ijms-25-06921-g004.jpg

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Not only metformin, but also D-allulose, alleviates metabolic disturbance and cognitive decline in prediabetic rats.
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d-Allulose is a substrate of glucose transporter type 5 (GLUT5) in the small intestine.d-阿洛酮糖是小肠葡萄糖转运蛋白 5 (GLUT5) 的底物。
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