在HFD小鼠中通过生物活性ETLVK和肠道微生物群减少后生物介导的肥胖
Jia-Yi Da1,2, Chang Wang1, Xiaomin Feng1
1Key Laboratory of Industrial Fermentation Microbiology of the Ministry of Education, College of Biotechnology, Tianjin University of Science and Technology, Tianjin 300457, China.
Journal of agricultural and food chemistry
|August 26, 2025
概括
通过改善脂质状况和减少炎症,抗击肥胖. 一个关键的,ETLVK,被确定为负责降脂效应,揭示了基于益生菌的代谢调节机制.
科学领域:
- 微生物学
- 代谢健康
- 益生菌
背景情况:
- 乳植物菌TCCC11824具有抗肥胖性质,但其活性成分尚未得到充分了解.
- 肥胖是一种复杂的代谢障碍,对健康有重大影响.
研究的目的:
- 调查L. plantarum TCCC11824压碎的超物 (LpS) 的抗肥胖机制.
- 确定对观察到的抗肥胖作用负责的特定生物活性成分.
主要方法:
- 高脂肪饮食 (HFD) 诱导的肥胖小鼠模型.
- 分析血液脂质,肝损伤和炎症标志物.
- 在体外酶抑制测定 (胰腺胆固醇酶和脂酶).
- 生物信息分析和LC-MS/MS用于的识别.
主要成果:
- 在肥胖小鼠中,LpS显著改善了脂质特征,减少了肝损伤和抑制了炎症.
- 减轻子宫外脂肪积累和调节肠道微生物群.
- 一个3-10kDa的LpS抑制了关键的脂质代谢酶和抑制了HMGCR的表达.
- 鉴定出ETLVK是降脂效应的主要媒介.
结论:
- 通过其上游剂 (LpS),L. plantarum TCCC11824具有广泛的抗肥胖作用.
- 微生物衍生的,特别是ETLVK,在降脂和抗肥胖活动中起着至关重要的作用.
- 这项研究为基于益生菌的代谢调节提供了洞察力.
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