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脂肪细胞ZAG通过重塑脂肪组织中的巨细胞群来改善肥胖引起的胰岛素耐药性

Zhezhen Liao¹, Yadi Wang¹, Can Hu¹

¹The First Affiliated Hospital of University of South China, Department of Metabolism and Endocrinology, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, China.

International immunopharmacology

|March 11, 2025

概括

脂肪组织 -α2-糖蛋白 (ZAG) 通过调节巨细胞两极分化来改善胰岛素敏感性. 失去ZAG会使炎症和胰岛素抵抗在肥胖中恶化,强调ZAG.

科学领域:

免疫代谢过程中的免疫代谢.
脂肪组织生物学脂肪组织生物学
肥胖研究的研究.

背景情况:

脂肪组织巨细胞 (ATM) 在肥胖中极大地影响代谢炎症和胰岛素敏感性.
了解脂肪细胞和巨细胞之间的阿迪波金介导的交叉声对代谢健康至关重要.
-α2-糖蛋白 (ZAG) 是一种抗炎性阿迪波金,与肥胖相关的代谢疾病有关.

研究的目的:

研究脂肪ZAG在代谢炎症中的特定作用.
阐明ZAG影响肥胖相关胰岛素抵抗的机制.
探索ZAG,胰岛素敏感性和巨细胞两极分化之间的关系.

主要方法:

对OMental ZAG与胰岛素敏感性和M2巨细胞标记物的相关性分析.
在高脂肪饮食的小鼠脂肪细胞中进行ZAG特异性切除,以评估代谢炎症.
评估M1巨细胞的比例和AKT信号通路的激活.
在体外实验中使用RAW264.7巨细胞研究ZAG通过特定信号通路对M1极化的影响.

主要成果:

口腔ZAG水平与胰岛素敏感性和M2巨细胞标记物正相关.
在高脂肪饮食中的小鼠中,脂肪细胞特异性的ZAG缺乏症加剧了胰岛素抵抗和脂肪组织炎症.
ZAG缺乏导致M1巨细胞比例增加,并抑制了AKT信号通路.
外源性ZAG通过β3-AR/PKA/STAT3信号通路抑制了palmitate诱导的M1巨分极.

结论:

来自脂肪细胞的ZAG在维持胰岛素敏感性方面起着保护作用.
ZAG通过影响巨细胞两极分化来调节脂肪组织炎症.
通过与脂肪定居的巨细胞交叉交流,ZAG维持胰岛素敏感性,影响肥胖的代谢健康.

关键词:

脂肪组织的脂肪组织.炎症炎症是一种炎症.胰岛素耐药性胰岛素耐药性是一种巨细胞是一个巨细胞.肥胖问题肥胖问题在 ZAGAG 的位置上.

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