肠道微生物群驱动的 BCAA 生物合成通过 Staphylococcus aureus - - 表达的乙酸盐合成酶损害了中国南部2型糖尿病的血糖控制
Tingting Liang1, Tong Jiang2, Zhuang Liang3
1Guangdong Provincial Key Laboratory of Microbial Safety and Health, State Key Laboratory of Applied Microbiology Southern China, Guangdong Institute of Microbiology, Guangdong Academy of Sciences, Guangzhou, China; Department of Clinical Laboratory Medicine, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China.
Microbiological research
|March 26, 2025
概括
增加的分支链氨基酸 (BCAA) 与2型糖尿病 (T2D) 胰岛素抵抗有关. 黄金葡萄球菌产生乙烯酸乳酸合成酶 (ALS) 被确定为一种原因,为糖尿病提供了新的治疗点.
科学领域:
- 微生物学 微生物学
- 代谢学 代谢学 代谢学
- 内分泌学 在内分泌学.
背景情况:
- 增加的分支链氨基酸 (BCAA) 水平与2型糖尿病 (T2D) 的胰岛素抵抗有关,但根本原因尚不清楚.
- 肠道微生物组的改变可能导致在不同T2D阶段观察到的不同临床特征.
研究的目的:
- 研究肠道微生物和代谢物在T2D病变发生过程中的作用.
- 确定导致糖尿病前期 (PDM),新诊断糖尿病 (NDDM) 和药后2型糖尿病 (P2DM) 胰岛素抵抗的特定微生物因素.
主要方法:
- 在T2D频谱中对患者进行元基因组学和代谢学分析.
- 微生物组成,代谢物水平和临床参数 (禁食血糖,胰岛素抵抗) 之间的相关性分析.
- 在小鼠模型中进行人性化的微生物移植和菌体治疗实验.
主要成果:
- 黄金葡萄球菌,特别是对乙烯酸乳酸合成酶 (ALS) 阳性菌株,在T2D患者中增加,特别是在P2DM组.
- 阳性ALS黄金菌与较高的BCAA水平,禁食血糖 (FBG) 和胰岛素抵抗相关.
- 胰岛素的使用被确定为T2D中S. aureus感染的潜在风险因素.
- 移植ALS阳性黄金色杆菌的微生物群在小鼠中诱导了胰岛素抵抗.
- 黄金菌体治疗降低了糖尿病小鼠的FBG和胰岛素抵抗.
结论:
- 黄球菌中的乙酸盐合成酶 (ALS) 是推动BCAA升高和T2D中的胰岛素耐药性的关键因素.
- 增加S. aureus的殖民化与T2D进展和胰岛素抵抗有关.
- 准ALS阳性黄金菌,可能通过菌体疗法,为T2D提供了一种新的治疗策略.
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