Diet and Gut Microbes Act Coordinately to Enhance Programmed Cell Death and Reduce Colorectal Cancer Risk.
Diet and Gut Microbes Act Coordinately to Enhance Programmed Cell Death and Reduce Colorectal Cancer Risk.
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饮食和肠道微生物协调作用，以增强程序性细胞死亡并降低结直肠癌风险。
DOI：
10.1007/s10620-020-06106-8
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发表时间：
2020-03
影响因子：
3.1
通讯作者：
Lampe JW
中科院分区：
文献类型：
--
作者：
Chapkin RS;Navarro SL;Hullar MAJ;Lampe JW
饮食是结直肠癌（CRC）的一个重要危险因素，与CRC有关的几种饮食成分被肠道微生物代谢改变。膳食纤维的微生物发酵产生短链脂肪酸，例如，乙酸、丙酸和丁酸。膳食纤维已被证明可以减少动物模型中的结肠肿瘤，并且在体外，丁酸盐影响对癌症风险很重要的细胞途径。此外，我们小组的工作表明，丁酸和ω-3多不饱和脂肪酸（n-3 PUFA）的联合作用可能会增强这些饮食成分的化学预防潜力。我们推测，西方人群中n-3 PUFA和纤维的摄入量相对较低，以及未能解决这些饮食成分之间的相互作用，这可能解释了为什么在前瞻性队列研究中没有一致地检测到n-3 PUFA和可发酵纤维的化学保护作用。在这篇综述中，我们总结的证据概述了n-3长链PUFA和高度发酵纤维的影响，相对于重要的CRC预防的关键途径的改变，特别是内在的神经细胞介导的程序性细胞死亡所造成的脂质活性氧的积累（ferroptosis），和表观遗传编程相关的脂质catalysts和β-氧化相关基因。
Diet is an important risk factor for colorectal cancer (CRC) and several dietary constituents implicated in CRC are modified by gut microbial metabolism. Microbial fermentation of dietary fiber produces short chain fatty acids, e.g., acetate, propionate, and butyrate. Dietary fiber has been shown to reduce colon tumors in animal models and, in vitro, butyrate influences cellular pathways important to cancer risk. Furthermore, work from our group suggests that the combined effects of butyrate and omega-3 polyunsaturated fatty acids (n-3 PUFA) may enhance the chemopreventive potential of these dietary constituents. We postulate that the relatively low intakes of n-3 PUFA and fiber in Western populations and the failure to address interactions between these dietary components may explain why chemoprotective effects of n-3 PUFA and fermentable fibers have not been detected consistently in prospective cohort studies. In this review, we summarize the evidence outlining the effects of n-3 long-chain PUFA and highly fermentable fiber with respect to alterations in critical pathways important to CRC prevention, particularly intrinsic mitochondrial-mediated programmed cell death resulting from the accumulation of lipid reactive oxygen species (ferroptosis), and epigenetic programming related to lipid catabolism and beta-oxidation associated genes.
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影响因子：
4.2
作者：
Cho, Youngmi;Kim, Hyemee;Lupton, Joanne R.
通讯作者：
Lupton, Joanne R.
Warburg效应决定了丁酸酯介导的组蛋白乙酰化和细胞增殖的机制。
影响因子：
16
作者：
Donohoe, Dallas R.;Collins, Leonard B.;Wali, Aminah;Bigler, Rebecca;Sun, Wei;Bultman, Scott J.
通讯作者：
Bultman, Scott J.
影响因子：
--
作者：
Chapkin, Robert S;DeClercq, Vanessa;Kim, Eunjoo;Fuentes, Natividad Roberto;Fan, Yang-Yi
通讯作者：
Fan, Yang-Yi
影响因子：
29
作者：
Donohoe DR;Garge N;Zhang X;Sun W;O'Connell TM;Bunger MK;Bultman SJ
通讯作者：
Bultman SJ
影响因子：
64.8
作者：
Arumugam, Manimozhiyan;Raes, Jeroen;Pelletier, Eric;Le Paslier, Denis;Yamada, Takuji;Mende, Daniel R.;Fernandes, Gabriel R.;Tap, Julien;Bruls, Thomas;Batto, Jean-Michel;Bertalan, Marcelo;Borruel, Natalia;Casellas, Francesc;Fernandez, Leyden;Gautier, Laurent;Hansen, Torben;Hattori, Masahira;Hayashi, Tetsuya;Kleerebezem, Michiel;Kurokawa, Ken;Leclerc, Marion;Levenez, Florence;Manichanh, Chaysavanh;Nielsen, H. Bjorn;Nielsen, Trine;Pons, Nicolas;Poulain, Julie;Qin, Junjie;Sicheritz-Ponten, Thomas;Tims, Sebastian;Torrents, David;Ugarte, Edgardo;Zoetendal, Erwin G.;Wang, Jun;Guarner, Francisco;Pedersen, Oluf;de Vos, Willem M.;Brunak, Soren;Dore, Joel;Weissenbach, Jean;Ehrlich, S. Dusko;Bork, Peer
通讯作者：
Bork, Peer