高脂饮食诱发结直肠癌期间宿主与肠道微生物群之间的代谢相互作用

IF 4.3 3区 材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC
Chaeeun Lee, Seungrin Lee, Woongjae Yoo
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引用次数: 0

摘要

结肠直肠癌(CRC)是全球男性和女性癌症相关死亡率第二高的原因。肥胖是导致 CRC 的风险因素之一,而肥胖与西方饮食习惯中盛行的高脂肪饮食有关。几十年来,肥胖性高脂肪饮食与 CRC 之间的关联已经确立;然而,高脂肪饮食增加 CRC 风险的机制仍不清楚。最近的研究表明,肠道微生物群对高脂饮食引起的肥胖和 CRC 的发病机制有很大影响。肠道微生物群由数百种细菌组成,其中一些与 CRC 有关。其中,兼性厌氧肠杆菌科细菌的扩增被认为是肠道微生物群功能失衡(菌群失调)的微生物特征,与高脂饮食诱发的肥胖和 CRC 都有关联。在此,我们将回顾高脂饮食诱发肥胖期间肠道微生物群及其代谢副产品与结直肠癌(CRC)之间的相互作用。此外,我们还将介绍在肠道炎症条件下,高脂饮食如何通过改变肠道上皮细胞的新陈代谢来推动产生基因毒性的大肠埃希氏菌的繁殖。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Metabolic Interaction Between Host and the Gut Microbiota During High-Fat Diet-Induced Colorectal Cancer

Metabolic Interaction Between Host and the Gut Microbiota During High-Fat Diet-Induced Colorectal Cancer

Colorectal cancer (CRC) is the second-highest cause of cancer-associated mortality among both men and women worldwide. One of the risk factors for CRC is obesity, which is correlated with a high-fat diet prevalent in Western dietary habits. The association between an obesogenic high-fat diet and CRC has been established for several decades; however, the mechanisms by which a high-fat diet increases the risk of CRC remain unclear. Recent studies indicate that gut microbiota strongly influence the pathogenesis of both high-fat diet-induced obesity and CRC. The gut microbiota is composed of hundreds of bacterial species, some of which are implicated in CRC. In particular, the expansion of facultative anaerobic Enterobacteriaceae, which is considered a microbial signature of intestinal microbiota functional imbalance (dysbiosis), is associated with both high-fat diet-induced obesity and CRC. Here, we review the interaction between the gut microbiome and its metabolic byproducts in the context of colorectal cancer (CRC) during high-fat diet-induced obesity. In addition, we will cover how a high-fat diet can drive the expansion of genotoxin-producing Escherichia coli by altering intestinal epithelial cell metabolism during gut inflammation conditions.

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来源期刊
CiteScore
7.20
自引率
4.30%
发文量
567
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