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膳食植物中的酚类提取物通过涉及 GLUT5 调节 Caco-2 细胞中果糖摄取。

Phenolics-Rich Extracts of Dietary Plants as Regulators of Fructose Uptake in Caco-2 Cells via GLUT5 Involvement.

机构信息

Faculty of Biotechnology and Food Sciences, Institute of Molecular and Industrial Biotechnology, Lodz University of Technology, Stefanowskiego 2/22, 90-537 Łódź, Poland.

Faculty of Biotechnology and Food Sciences, Institute of Natural Products and Cosmetics, Lodz University of Technology, Stefanowskiego 2/22, 90-537 Łódź, Poland.

出版信息

Molecules. 2021 Aug 5;26(16):4745. doi: 10.3390/molecules26164745.

DOI:10.3390/molecules26164745
PMID:34443333
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8401051/
Abstract

The latest data link the chronic consumption of large amounts of fructose present in food with the generation of hypertension and disturbances in carbohydrate and lipid metabolism, which promote the development of obesity, non-alcoholic fatty liver disease, insulin resistance, and type 2 diabetes. This effect is possible after fructose is absorbed by the small intestine cells and, to a lesser extent, by hepatocytes. Fructose transport is dependent on proteins from the family of glucose transporters (GLUTs), among which GLUT5 selectively absorbs fructose from the intestine. In this study, we examined the effect of four phenolic-rich extracts obtained from , , and on fructose uptake by Caco-2 cells. Extracts from and most effectively reduced fluorescent fructose analogue (NBDF) accumulation in Caco-2, as well as downregulated GLUT5 protein levels. These preparations were able to decrease the mRNA level of genes encoding transcription factors regulating GLUT5 expression-thioredoxin-interacting protein (TXNIP) and carbohydrate-responsive element-binding protein (ChREBP). Active extracts contained large amounts of apigenin and flavonols. The molecular docking simulation suggested that some of identified phenolic constituents can play an important role in the inhibition of GLUT5-mediated fructose transport.

摘要

最新数据表明,大量存在于食物中的果糖的慢性消耗与高血压的产生以及碳水化合物和脂质代谢紊乱有关,这些会促进肥胖、非酒精性脂肪肝、胰岛素抵抗和 2 型糖尿病的发展。这种效应可能是在果糖被小肠细胞吸收后发生的,在较小程度上也可能是被肝细胞吸收后发生的。果糖的转运依赖于葡萄糖转运蛋白(GLUTs)家族的蛋白质,其中 GLUT5 选择性地从肠道吸收果糖。在这项研究中,我们研究了从 、 、 和 中获得的四种富含酚类的提取物对 Caco-2 细胞摄取果糖的影响。 和 提取物最有效地减少了 Caco-2 中荧光果糖类似物(NBDF)的积累,并下调了 GLUT5 蛋白水平。这些制剂能够降低编码调节 GLUT5 表达的转录因子的基因的 mRNA 水平-硫氧还蛋白相互作用蛋白(TXNIP)和碳水化合物反应元件结合蛋白(ChREBP)。活性提取物含有大量的芹菜素和类黄酮。分子对接模拟表明,一些已鉴定的酚类成分可能在抑制 GLUT5 介导的果糖转运中发挥重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/02d8/8401051/521e47b79b81/molecules-26-04745-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/02d8/8401051/1728202361ef/molecules-26-04745-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/02d8/8401051/b870a3a881e1/molecules-26-04745-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/02d8/8401051/1a846cf3122a/molecules-26-04745-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/02d8/8401051/23fcbd6f6859/molecules-26-04745-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/02d8/8401051/dc1c0841a6f4/molecules-26-04745-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/02d8/8401051/d40ec9139cf0/molecules-26-04745-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/02d8/8401051/a0106db604a5/molecules-26-04745-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/02d8/8401051/cebfe96d3bec/molecules-26-04745-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/02d8/8401051/3a894da96712/molecules-26-04745-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/02d8/8401051/521e47b79b81/molecules-26-04745-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/02d8/8401051/1728202361ef/molecules-26-04745-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/02d8/8401051/b870a3a881e1/molecules-26-04745-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/02d8/8401051/1a846cf3122a/molecules-26-04745-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/02d8/8401051/23fcbd6f6859/molecules-26-04745-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/02d8/8401051/dc1c0841a6f4/molecules-26-04745-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/02d8/8401051/d40ec9139cf0/molecules-26-04745-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/02d8/8401051/a0106db604a5/molecules-26-04745-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/02d8/8401051/cebfe96d3bec/molecules-26-04745-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/02d8/8401051/3a894da96712/molecules-26-04745-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/02d8/8401051/521e47b79b81/molecules-26-04745-g010.jpg

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