基因饮食诱导的胆酸通过减少卡路里吸收来防止肥胖
Xiao Li1, Jie Yang1, Xiaofeng Zhou1
1State Key Laboratory of Genetic Engineering, School of Life Sciences, Human Phenome Institute, Fudan University, Shanghai, P.R. China.
Nature metabolism
|June 27, 2024
概括
性饮食 (KD) 改变了肠道细菌,增加了像 taurodeoxycholic 酸 (TDCA) 和 tauroursodeoxycholic 酸 (TUDCA) 这样的胆酸. 这种机制有助于减肥,并通过减少能量吸收来降低葡萄糖.
科学领域:
- 微生物学 微生物学
- 代谢过程中的代谢.
- 胃肠病学 胃肠病学
背景情况:
- 低碳水化合物类饮食 (KD) 用于减肥,但其机制尚未完全理解.
- 肠道微生物群和代谢物与KD的代谢作用有关,但具体的微生物或代谢介质仍然不清楚.
研究的目的:
- 阐明KD消费如何影响体重和血糖水平的机制.
- 为了确定特定的肠道微生物和参与KD诱导的代谢变化的代谢物.
主要方法:
- 研究KD对小鼠血清胆汁酸水平 (TDCA,TUDCA) 和肠道微生物群组成的影响.
- 研究了Lactobacillus murinus ASF361及其胆盐化酶 (BSH) 活性在介导KD效应中的作用.
- 评估了TDCA和TUDCA对肠道碳酸酶1的表达和能量吸收的影响.
- 在观察性和干预性人类研究中得到验证的结果.
主要成果:
- 在小鼠中,KD消费增加了血清TDCA和TUDCA水平,与体重减轻和禁食葡萄糖相关.
- 在KD养中,BSH编码的Lactobacillus murinus ASF361.1.的丰度下降.
- 减少L. murinus ASF361或BSH抑制导致更高的TDCA/TUDCA,抑制碳酸 anhydrase 1并降低能量吸收.
- 在小鼠模型中,TDCA和TUDCA治疗证明了对肥胖的保护作用.
- 胆酸,微生物BSH和代谢特征之间的关联在人类研究中得到证实.
结论:
- 发现了一种新的宿主-肠道微生物群相互作用机制,用于KD介导的体重减轻和降低葡萄糖.
- 确定了TDCA和TUDCA作为关键调解者,将KD,肠道微生物群和代谢改善联系起来.
- TDCA和TUDCA显示出作为治疗肥胖和相关并发症的治疗剂的潜力.
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