在脂肪组织巨细胞中恢复 lysosomes 缓解肥胖引起的炎症和胰岛素抵抗
Jiyeon Chang1,2, Ellen Budiono1,2, Shindy Soedono1,2
1Department of Integrated Biomedical Science, Soonchunhyang University, Cheonan 31151, Republic of Korea.
International journal of molecular sciences
|February 27, 2026
概括
肥胖导致脂肪组织巨细胞 (ATM) 的溶酶体功能障碍,损害代谢健康. 使用HPβCD恢复 lysosomal功能改善了葡萄糖耐受性和减少了炎症,这表明代谢性疾病的治疗点.
科学领域:
- 代谢性炎症是一种代谢性炎症.
- 溶酶体生物学 溶酶体生物学
- 肥胖的病原体是肥胖的病原体.
背景情况:
- 脂肪组织巨细胞 (ATM) 驱动与肥胖相关的炎症和胰岛素抵抗.
- Lysosomal 功能障碍在 ATM 炎症激活中的作用尚不清楚.
研究的目的:
- 描述肥胖期间ATM的溶酶体变化.
- 调查HPβCD是否可以恢复 lysosomal 功能并改善代谢炎症.
主要方法:
- 饮食诱导的肥胖小鼠模型.
- 溶解体功能测定 (酸化,酶表达).
- HPβCD治疗和代谢评估 (耐葡萄糖,胰岛素敏感性).
- 流细胞测量用于免疫细胞分析.
- 在体外巨细胞激活研究.
主要成果:
- 肥胖的ATM显示 lysosomal 含量增加,但酸化受损并减少TFEB表达.
- HPβCD治疗改善了葡萄糖耐受性和胰岛素敏感性.
- 在内脏脂肪组织中,HPβCD减少了促炎M1ATM和CD8+T细胞.
- 在宏细胞中,HPβCD抑制了炎症基因表达,并在体外恢复了TFEB.
结论:
- 肥胖引起的ATM中的溶酶体功能障碍有助于代谢疾病.
- 通过HPβCD恢复 lysosomal 功能可以缓解脂肪组织炎症和代谢功能障碍.
- 在ATM中溶解体调节为肥胖相关的代谢障碍提供了潜在的治疗策略.
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