Adipocyte ZAG improves obesity-triggered insulin resistance by reshaping macrophages populations in adipose tissue.

• Tác giả: Qianqian Gu, Can Hu, Zhezhen Liao, Ting Peng, Li Ran, Qiyu Wang, Yadi Wang, Yuanyuan Wang, Liangliang Wu, Xinhua Xiao, Liyong Zhu
• Ngôn ngữ: eng
• Ký hiệu phân loại: 598.413 *Anas
• Thông tin xuất bản: Netherlands : International immunopharmacology , 2025
• Bộ sưu tập: NCBI
• ID: 695506

Tóm tắt

Adipose tissues macrophages (ATMs) serve as a critical effector in the mediating occurrence of metabolic inflammation to impact whole-body insulin sensitivity in obesity. Discovering the key adipokines mediating crosstalk of adipocytes-macrophages and understanding the molecular mechanism of ATMs polarization and function have become hot topic issues in the immunometabolism fields. Zinc-α2-glycoprotein (ZAG) as a anti-inflammatory adipokines plays important roles in obesity-related metabolic diseases. We attempt to explore the precise role of adipose ZAG in metabolic inflammation and obesity-associated insulin resistance. Here we showed that Omental ZAG was positively associated with insulin sensitivity and M2 macrophages markers. ZAG-specific ablation in adipocyte aggravated insulin resistance and adipose tissues inflammation as evidenced by enhanced M1 macrophages proportion and inhibited AKT signaling pathway in mice fed with a high-fat diet. Exogenous ZAG inhibits PA-induced M1 macrophage polarization via β3-AR/PKA/STAT3 signaling in RAW264.7 macrophages.These findings suggest that adipocyte ZAG maintain insulin sensitivity via the cross talk with adipose-resident macrophages.