HIF-1减弱了高纤维饮食中介的结肠表皮的增殖和干性
Pollyana Ribeiro Castro1, Renan Oliveira Corrêa1,2, Monara Kaélle Sérvulo Cruz Angelim3
1Laboratory of Immunoinflammation, Department of Genetics, Evolution, Microbiology and Immunology, Institute of Biology, University of Campinas, Campinas, SP, Brazil.
Gut microbes
|August 19, 2025
概括
像胰岛素这样的食纤维促进肠道缺氧,并稳定肠道细胞中的缺氧诱导因子1 (HIF-1). 这一过程依赖于肠道微生物,影响干细胞功能和结肠上皮代谢.
科学领域:
- 微生物学和宿主免疫相互作用
- 胃肠道生理学 胃肠道生理学
- 营养科学 营养科学
背景情况:
- 食纤维显著影响肠道微生物群和宿主生理学.
- 溶解纤维的胰岛素诱导由微生物产品介导的结肠上皮细胞变化.
- 了解饮食-微生物群-宿主相互作用对于肠道健康至关重要.
研究的目的:
- 调查胰岛素对肠道缺氧和肠道上皮细胞 (IEC) 中HIF-1信号传递的影响.
- 探索微生物群和宿主因子在调解这些影响中的作用.
- 阐明HIF-1稳定如何影响肠干细胞 (ISC) 功能和新陈代谢.
主要方法:
- 采用了多种omics方法,结合了饮食干预和肠道器官.
- 利用遗传和药理干预来研究缺氧诱导因子1 (HIF-1) 信号传递.
- 评估了对肠道上皮细胞 (IEC) 的微生物群和宿主依赖的影响.
主要成果:
- 摄入胰岛素可以促进肠道缺氧,并稳定IEC中的HIF-1.
- 这种稳定性取决于宿主和肠道微生物群.
- HIF-1稳定通过微生物群依赖的代谢重编程来调节ISC功能.
结论:
- 胰岛素是一种可溶性纤维,在调节肠道缺氧和HIF-1信号传递方面发挥着重要作用.
- HIF-1 作为微生物群依赖的表皮代谢和结肠中的增殖的关键调解者.
- 这些发现强调了HIF-1在复杂的饮食-微生物群-宿主轴中未被认可的作用.
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