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肠道微生物群通过巨细胞衰老和格兰卡尔辛分泌调节与肥胖相关的骨恶化

Min Huang^1,2, Mei Huang¹, Ling Liu¹

¹Department of Endocrinology, Endocrinology Research Center, Xiangya Hospital, Central South University, Changsha, 410008, China.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)

|May 11, 2025

概括

肥胖会通过改变肠道微生物来恶化骨健康,这些微生物会导致老化的骨髓巨细胞 (BMM) 释放格兰卡辛 (GCA). 准这些细胞和GCA可能会保护肥胖个体的骨.

科学领域:

免疫学免疫学免疫学
微生物学微生物学
骨生物学骨生物学骨生物学

背景情况:

肥胖与骨质恶化和骨折风险更高有关.
驱动与肥胖相关的骨衰退的精确机制在很大程度上是未知的.
肠道微生物群的组成在肥胖中发生变化,影响全身健康.

研究的目的:

阐明肠道微生物群在肥胖引起的骨恶化中的作用.
研究骨髓巨细胞 (BMM) 和花素 (GCA) 在这个过程中的参与.
确定潜在的治疗目标,以保持肥胖患者的骨健康.

主要方法:

使用肥胖小鼠模型和便微生物群移植 (FMT).
评估了骨髓中的BMM衰老和GCA表达.
在人类参与者 (n=40) 中分析了血清GCA水平.
研究了来自肠道微生物群的脂聚糖 (LPS) 通过托尔类受体4 (TLR4) 刺激GCA的机制.
使用Gca基因缺乏的小鼠和GCA中和抗体.

主要成果:

肥胖小鼠和接受肥胖FMT的小鼠表现出老化BMM的增加和骨髓GCA的升高.
肥胖的人类参与者表现出较高的血清GCA水平.
肥胖肠道微生物群衍生的LPS激活了老化的BMM中的TLR4,增加了GCA表达.
Gca基因删除赋予了对肥胖和LPS诱导的骨损伤的抵抗力.
GCA 中和改善了肥胖小鼠和LPS诱导的炎症模型中的骨恶化.

结论:

肥胖肠道微生物群通过诱导BMM衰老和GCA分泌来驱动骨恶化.
肠道微生物群与免疫系统的相互作用在与肥胖相关的骨质损失中至关重要.
准衰老的巨细胞和GCA是一个有希望的策略,用于保护肥胖的骨健康.

关键词:

石灰质石灰质石灰质石灰质石灰质我们的肠道微生物群.免疫性免疫性免疫性肥胖肥胖肥胖肥胖肥胖肥胖肥胖肥胖骨的恶化骨的恶化

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