层次的糖解路径控制人类肠道中的碳水化合物利用调节器细菌体
Seth G Kabonick1,2,3, Kamalesh Verma1,2,3, Jennifer L Modesto1,2,3
1Penn State College of Medicine, Hershey, PA, USA.
bioRxiv : the preprint server for biology
|November 28, 2024
概括
像葡萄糖和果糖这样的简单糖通过抑制碳水化合物利用调节器 (Cur) 来破坏肠道细菌. 这个过程需要依赖ATP的果糖-1,6-双酸盐合成,影响宿主健康.
科学领域:
- 微生物学 微生物学
- 人类肠道微生物组
- 细菌的新陈代谢
背景情况:
- 人类饮食中含有高简单糖的食物会影响肠道微生物群.
- 肠道微生物组的破坏与肠道疾病有关.
- 在 *Bacteroidetes* 中,碳水化合物利用调节器 (Cur) 控制着关键的细菌功能.
研究的目的:
- 阐明简单糖抑制哺乳动物肠道Cur活性的机制.
- 为了研究ATP依赖的果糖-1,6-双酸盐 (FBP) 合成在糖诱导的Cur抑制中的作用.
- 了解对 *Bacteroides* 健身和对宿主有益的产品的影响.
主要方法:
- 研究了葡萄糖和果糖对*Bacteroides*物种*Cur活性的影响.
- 评估了依赖ATP的FBP合成对于Cur抑制的必要性.
- 与Cur和没有Cur的细菌生长和健康状况进行比较,检查酸盐 (PPi) 依赖酶的作用.
主要成果:
- 对于葡萄糖或果糖来说,依赖ATP的FBP合成是必不可少的,以抑制Cur中的*细菌体*.
- 这种依赖ATP的途径对于细菌生长是不可或缺的,因为有另一种依赖PPi的酶.
- 依赖ATP的FBP合成对于肠道Cur调节至关重要,但当Cur缺少时,对于细菌的适应性至关重要.
结论:
- 简单糖通过依赖ATP的FBP合成抑制了肠道中的Cur活性.
- 这种抑制会破坏*细菌体*的适应性,并减少有益的宿主相关产品.
- 当Cur缺少时,酸盐 (PPi) 足以支持*Bacteroides*中的糖解.
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