高脂肪饮食通过改变肠道微生物的酸盐代谢来促进结肠炎相关的瘤发生
Xinyu Shao1,2, Luojie Liu3, Yuqing Zhou2
1Department of Gastroenterology, The First Affiliated Hospital of Soochow University, Suzhou 215006, Jiangsu, China.
International journal of biological sciences
|October 2, 2023
概括
高脂肪饮食通过破坏肠道细菌和减少丁酸盐来促进结肠炎相关的癌症. 用丁酸盐补充剂逆转了这些影响,为结肠炎相关的癌症提供了潜在的治疗方法.
科学领域:
- 微生物学 微生物学
- 在瘤学瘤学.
- 免疫学 免疫学 免疫学
背景情况:
- 摄入高脂肪饮食 (HFD) 与结肠炎相关癌症 (CAC) 的风险增加有关.
- HFD诱导全身低度炎症,特别是在结肠中,由亲炎性巨细胞驱动,从而加速CAC的进展.
- 这项研究调查了HFD如何通过改变肠道微生物的酸盐代谢来影响CAC.
研究的目的:
- 通过肠道微生物酸盐代谢的修改,探索HFD在驱动CAC中的作用.
- 研究由HFD诱导的CAC背后的机制,重点关注肠道微生物群,酸盐代谢和NLRP3炎症酶途径.
主要方法:
- 使用HFD治疗和便微生物种移植 (FMT) 调查了HFD诱导的肠道微生物群变化.
- 在CAC小鼠模型中分析了肠道微生物群组成,短链脂肪酸 (SCFA) 水平和NLRP3炎症酶激活.
- 进行了体外实验,用脂多糖和丁酸盐治疗巨细胞,以评估M1极化和NLRP3/Caspase-1通路表达.
主要成果:
- 在小鼠中,HFD加速了CAC的进展,这种效应被广谱抗生素逆转.
- 高酸减少了生产丁酸盐的细菌的丰富性,并降低了肠道丁酸盐水平.
- 外源性丁酸盐的使用逆转了HFD诱导的M1巨分化,肠道炎症和瘤生长,同时抑制了NLRP3/Caspase-1通路.
结论:
- HFD促进结肠炎相关的瘤发生,通过引起肠道失调和抑制丁酸盐代谢,导致扭曲的巨细胞两极分化.
- 外源性丁酸盐是结肠炎相关癌症的有希望的治疗策略,具有临床应用的潜力.
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