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在果糖存在的情况下,卵清蛋白消化过程中会形成晚期糖基化终产物:绿原酸的抑制作用。

Advanced glycation endproducts form during ovalbumin digestion in the presence of fructose: Inhibition by chlorogenic acid.

作者信息

Bains Yasmin, Gugliucci Alejandro, Caccavello Russell

机构信息

Glycation, Oxidation and Disease Laboratory, Dept. of Research, College of Osteopathic Medicine, Touro University-California, Vallejo, CA, USA.

Glycation, Oxidation and Disease Laboratory, Dept. of Research, College of Osteopathic Medicine, Touro University-California, Vallejo, CA, USA.

出版信息

Fitoterapia. 2017 Jul;120:1-5. doi: 10.1016/j.fitote.2017.05.003. Epub 2017 May 17.

DOI:10.1016/j.fitote.2017.05.003
PMID:28527897
Abstract

BACKGROUND

One mechanism by which fructose could exert deleterious effects is through intestinal formation and absorption of pro-inflammatory advanced glycation endproducts via the Maillard reaction. We employed simulated stomach and duodenum digestion of ovalbumin (OVA) to test the hypothesis that advanced glycation endproducts (AGEs) are formed by fructose during simulated digestion of a ubiquitous food protein under model physiological conditions.

METHODS

OVA was subjected to simulated gastric and intestinal digestion using standard models, in presence of fructose or glucose (0-100mM). Peptide fractions were analyzed by fluorescence spectroscopy and intensity at Excitation: λ370nm, Emission: λ 440nm.

RESULTS

AGE adducts formed between fructose and OVA, evidenced by the peptide fractions (<5kDa) at times (30min) and concentration ranges (10mM) plausibly found in the intestines, whereas no reaction occurs with glucose. The reaction was inhibited by chlorogenic acid at concentrations compatible with those found in the gut. The reaction was also inhibited by aminoguanidine, a specific antiglycation agent.

CONCLUSION

Our study showed fructose-AGE formation on a ubiquitous dietary protein under model physiological conditions. Our study also suggests ways to decrease the damage: enteral fructose-AGE formation may be partially inhibited by co-intake of beverages, fruits and vegetables with concentrations of phenolics high enough to serve as anti-glycation agents.

摘要

背景

果糖发挥有害作用的一种机制是通过美拉德反应在肠道中形成并吸收促炎性晚期糖基化终产物。我们采用卵清蛋白(OVA)的模拟胃和十二指肠消化来检验以下假设:在模拟生理条件下,果糖在一种普遍存在的食物蛋白的消化过程中会形成晚期糖基化终产物(AGEs)。

方法

使用标准模型在果糖或葡萄糖(0 - 100mM)存在的情况下对OVA进行模拟胃和肠道消化。通过荧光光谱法分析肽段,激发波长:λ370nm,发射波长:λ440nm。

结果

果糖与OVA之间形成了AGE加合物,在肠道中可能出现的时间(30分钟)和浓度范围(10mM)下,<5kDa的肽段可证明这一点,而葡萄糖则不会发生反应。绿原酸在与肠道中发现的浓度相当的情况下可抑制该反应。该反应也被氨基胍(一种特异性抗糖基化剂)抑制。

结论

我们的研究表明在模拟生理条件下,果糖会在一种普遍存在的膳食蛋白上形成AGE。我们的研究还提出了减少损害的方法:通过共同摄入酚类物质浓度足够高、可作为抗糖基化剂的饮料、水果和蔬菜,可能会部分抑制肠内果糖 - AGE的形成。

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