Fructose aggravating colon barrier dysfunction by decreasing gut bacteria metabolites indole-3-carboxaldehyde and inhibiting activation of aryl hydrocarbon receptor in vivo and in vitro  

作　　者：Ge Song Shaojie Pang Wenting Peng Wei Fang Yong Wang Rui Liu Qianyun Gan Wentao Qi 

机构地区：[1]Academy of National Food and Strategic Reserves Administration,Beijing 100037,China [2]Department of Nutrition and Food Hygiene,School of Public Health,Peking University,Beijing 100191,China [3]School of Health Science and Engineering,University of Shanghai for Science and Technology,Shanghai 200093,China

出　　处：《Food Science and Human Wellness》2025年第4期1480-1497,共18页食品科学与人类健康(英文)

基　　金：supported by the Special Funds of Basic Research of Central Public Welfare Institute(JY2010 and ZX2410)。

摘　　要：Background:Fructose may induce non-alcoholic fatty acids(NAFLD)due to the gut-liver axis interactions.The mechanism of fructose impairing colon barrier is unrevealed.Methods:Normal and dextran sulfate sodium(DSS)-induced Sprague-Dawley rats fed by 35%fructose diets were used to evaluate colon barrier functions.Microbiome and metabolome were applied to screen potential biomarker bacteria and metabolites induced by fructose.HT-29 cells were applied to validate metabolite biomarker indoleacrylic acid(IAA)and indole-3-carboxaldehyde(I3A)function in colon barrier which impaired by fructose.Results:Fructose induced colon barrier dysfunction,aggravated colon impairment in DSS-induced rats.With fructose intake,the colon length shortened,goblet numbers declined,inflammation infiltration induced,inflammatory cytokines increased,and apoptosis signals upregulated in colon tissue.Moreover,fructose induced dysbiosis of microbiota and their metabolites.Adlercreutzia and Holdemania were screened out as potential bacteria biomarkers,IAA and I3A as tryptophan metabolites were selected as metabolite biomarkers inhibited by fructose.IAA and I3A treatment alleviated the impairment induced by fructose by increasing trans epithelial electric resistance value,tight junction proteins,and Aryl hydrocarbon receptor(Ah R)activity in HT-29 cell.Conclusion:Fructose stimulated inflammation,apoptosis,gut bacteria alteration,and induced the reduction of IAA and I3A.Since fructose inhibited production of IAA and I3A,Ah R remained inactivated and consequently induced colon barrier dysfunction.

关 键 词：FRUCTOSE Tryptophan metabolites Colon barrier 

分 类 号：R57[医药卫生—消化系统]