Zheng Shimin, Yin Jianbin, Yue Hui, Li Lifu
Department of Gastroenterology and Hepatology, The Third Affiliated Hospital, Southern Medical University, Guangzhou, China.
The Third School of Clinical Medicine, Southern Medical University, Guangzhou, China.
Front Nutr. 2023 May 12;10:1191206. doi: 10.3389/fnut.2023.1191206. eCollection 2023.
A high-fat diet plays a key role in the pathogenesis of colorectal cancer, and this effect on the gut can also occur in the offspring of mothers with a high-fat diet. In this review, we discuss the role of a high-fat diet in the pathogenesis of colorectal cancer and summarize the effects of a maternal high-fat diet on the activation of inflammation and development of colorectal cancer in offspring. Studies have found that a maternal high-fat diet primarily induces an inflammatory response in the colorectal tissue of both the mother herself and the offspring during pregnancy. This leads to the accumulation of inflammatory cells in the colorectal tissue and the release of inflammatory cytokines, which further activate the NF-κb and related inflammatory signaling pathways. Research suggests that high levels of lipids and inflammatory factors from mothers with a high-fat diet are passed to the offspring through the transplacental route, which induces colorectal inflammation, impairs the intestinal microecological structure and the intestinal barrier, and interferes with intestinal development in the offspring. This in turn activates the NF-κb and related signaling pathways, which further aggravates intestinal inflammation. This process of continuous inflammatory stimulation and repair may promote the uncontrolled proliferation of colorectal mucosal cells in the offspring, thus increasing their susceptibility to colorectal cancer.
高脂饮食在结直肠癌的发病机制中起关键作用，这种对肠道的影响在高脂饮食母亲的后代中也会出现。在本综述中，我们讨论高脂饮食在结直肠癌发病机制中的作用，并总结母体高脂饮食对后代炎症激活和结直肠癌发展的影响。研究发现，母体高脂饮食主要在孕期诱导母亲自身及后代的结肠组织发生炎症反应。这导致结肠组织中炎症细胞积聚以及炎症细胞因子释放，进而激活NF-κb及相关炎症信号通路。研究表明，高脂饮食母亲体内的高水平脂质和炎症因子通过胎盘途径传递给后代，诱发结肠炎症，损害肠道微生态结构和肠道屏障，并干扰后代的肠道发育。这反过来又激活NF-κb及相关信号通路，进一步加重肠道炎症。这种持续的炎症刺激和修复过程可能促进后代结肠黏膜细胞的无节制增殖，从而增加其患结直肠癌的易感性。
