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

被引:30
|
作者
Bains, Yasmin [1 ]
Gugliucci, Alejandro [1 ]
Caccavello, Russell [1 ]
机构
[1] Touro Univ California, Coll Osteopath Med, Dept Res, Glycat Oxidat & Dis Lab, Vallejo, CA 94592 USA
关键词
Advanced glycation; Fructose; Inflammation; Ovalbumin; END-PRODUCTS; ILEX-PARAGUARIENSIS; CROSS-LINKING; CORN SYRUP; MALABSORPTION; RESTRICTION; BEVERAGES; CHILDREN; COLLAGEN; HEALTH;
D O I
10.1016/j.fitote.2017.05.003
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
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 (0-100 mM). Peptide fractions were analyzed by fluorescence spectroscopy and intensity at Excitation: lambda 370 nm, Emission: lambda 440 nm. Results: AGE adducts formed between fructose and OVA, evidenced by the peptide fractions (<5 kDa) at times (30 min) and concentration ranges (10 mM) 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.
引用
收藏
页码:1 / 5
页数:5
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