脂肪因子Metrnl在代谢性疾病中的研究进展

Research Progress of Fat Factor Metrnl in Metabolic Diseases

摘要: 肥胖、2型糖尿病、代谢相关脂肪性肝病、多囊卵巢综合征等代谢性疾病发病率逐年攀升，已成为全球重要公共卫生问题，其核心病理机制与胰岛素抵抗、糖脂代谢紊乱及多组织慢性低度炎症密切相关。Meteorin-like (Metrnl)是兼具脂肪因子与肌因子属性的新型多功能分泌蛋白，广泛表达于机体核心代谢器官，可通过AMPK、PPARγ、TLR4/NF-κB等多条通路，双向调控糖脂代谢与免疫炎症，阻断代谢紊乱恶性循环。近年研究证实，Metrnl在不同代谢性疾病及病程中存在表达异质性，可精准参与疾病发生、发展全过程，具备重要的诊疗参考价值。本文系统梳理国内外Metrnl相关基础与临床研究，总结其生物学特性、对各类代谢性疾病的调控作用及核心分子机制，剖析当前研究争议与临床转化瓶颈，展望其临床应用前景，旨在为代谢性疾病的机制研究、早期筛查及靶向治疗提供理论依据。

Abstract: The incidence rate of metabolic diseases, such as obesity, type 2 diabetes, metabolic fatty liver disease, polycystic ovary syndrome, has increased year by year, and has become an important global public health problem. Its core pathological mechanism is closely related to insulin resistance, glucose and lipid metabolism disorders, and chronic low-grade inflammation of multiple tissues. Meteorin like (Metrnl) is a novel multifunctional secreted protein that combines the properties of adipokines and myokines. It is widely expressed in the core metabolic organs of the body and can bidirectionally regulate glucose and lipid metabolism and immune inflammation through multiple pathways such as AMPK, PPARγ, TLR4/NF-κB, blocking the vicious cycle of metabolic disorders. In recent years, research has confirmed that there is heterogeneity in the expression of Metrnl in different metabolic diseases and disease courses, which can accurately participate in the entire process of disease occurrence and development, and has important diagnostic and therapeutic reference value. This article systematically reviews the basic and clinical research on Metrnl at home and abroad, summarizes its biological characteristics, regulatory effects on various metabolic diseases, and core molecular mechanisms. It analyzes the current research controversies and clinical translation bottlenecks, and looks forward to its clinical application prospects. The aim is to provide theoretical basis for the mechanism research, early screening, and targeted treatment of metabolic diseases.