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短链脂肪酸暴露后肠上皮样Caco-2细胞的差异调节

Differential modulation of enterocyte-like Caco-2 cells after exposure to short-chain fatty acids.

作者信息

Malago J J, Koninkx J F J G, Douma P M, Dirkzwager A, Veldman A, Hendriks H G C J M, van Dijk J E

机构信息

Department of Veterinary Pathology, Faculty of Veterinary Medicine, Utrecht University, The Netherlands.

出版信息

Food Addit Contam. 2003 May;20(5):427-37. doi: 10.1080/0265203031000137728.

Abstract

The response of intestinal epithelial cells to short-chain fatty acids, which are increasingly used as food additives, was investigated. Human small intestinal epithelial cell model Caco-2 cells were exposed to formate, propionate and butyrate to assess their effect on cellular growth, metabolism, differentiation and protection against bacteria. The Caco-2 cells were entirely grown in the different short-chain fatty acids and respective growth patterns were determined. Differentiated cells were exposed to 0-20 mM short-chain fatty acids for 48 h and changes in DNA, RNA, (glyco)protein syntheses, sucrase isomaltase activity, transepithelial electrical resistance and protection against Salmonella enteritidis were measured. The short-chain fatty acids, altered linearly and differentially the growth pattern ranging from stimulation by formate to inhibition by butyrate. Formate inhibited cellular metabolism. Low concentrations of up to 5 mM propionate and 2 mM butyrate stimulated metabolism, while higher doses were inhibitory. Formate had no effect on sucrase isomaltase enzyme activity and transepithelial electrical resistance, whereas propionate and butyrate increased these markers of differentiation. Infection with S. enteritidis did not benefit from the short-chain fatty acid-induced transepithelial electrical resistance. It is concluded that formate, propionate and butyrate selectively and differentially modulate growth characteristics, cellular metabolism, sucrase isomaltase activity and transepithelial electrical resistance in a concentration- and carbon atom-related fashion. The short-chain fatty acid-induced transepithelial electrical resistance does not confer protection against S. enteritidis.

摘要

研究了肠道上皮细胞对越来越多地用作食品添加剂的短链脂肪酸的反应。将人小肠上皮细胞模型Caco-2细胞暴露于甲酸、丙酸和丁酸中,以评估它们对细胞生长、代谢、分化以及对细菌的保护作用。Caco-2细胞完全在不同的短链脂肪酸中生长,并确定各自的生长模式。将分化的细胞暴露于0-20 mM的短链脂肪酸中48小时,并测量DNA、RNA、(糖)蛋白合成、蔗糖酶异麦芽糖酶活性、跨上皮电阻以及对肠炎沙门氏菌的保护作用的变化。短链脂肪酸线性且不同程度地改变了生长模式,从甲酸的刺激到丁酸的抑制。甲酸抑制细胞代谢。低浓度(高达5 mM的丙酸和2 mM的丁酸)刺激代谢,而高剂量则具有抑制作用。甲酸对蔗糖酶异麦芽糖酶活性和跨上皮电阻没有影响,而丙酸和丁酸增加了这些分化标志物。肠炎沙门氏菌感染并未从短链脂肪酸诱导的跨上皮电阻中受益。得出的结论是,甲酸、丙酸和丁酸以浓度和碳原子相关的方式选择性且不同程度地调节生长特性、细胞代谢、蔗糖酶异麦芽糖酶活性和跨上皮电阻。短链脂肪酸诱导的跨上皮电阻不能提供对肠炎沙门氏菌的保护作用。

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