Abstract: Type 2 diabetes mellitus (T2DM) is frequently accompanied by other features of metabolic syndrome, leading to vascular complications, end-stage organ failure, and cancer. Metabolic dysfunction-associated steatotic liver disease (MASLD) is one of the common complications of T2DM, with over 70% of T2DM patients also having MASLD. Peroxisome proliferator activated receptors (PPARs) participate in gene expression related to fatty acid uptake, β-oxidation, lipogenesis, gluconeogenesis, and insulin sensitivity. The pathogenesis of MASLD is closely associated with PPAR dysfunction, characterized by impaired fatty acid oxidation capacity, disrupted adipose tissue function, reduced insulin sensitivity, and abnormal activation of inflammatory signaling pathways. This review aims to elucidate the key mechanisms and pathophysiological roles of PPARs in T2DM and MASLD, providing a theoretical foundation for further research into PPAR-targeted therapies for this condition.

Key words: Metabolic dysfunction-associated steatotic liver disease, Diabetes mellitus, type 2, Peroxisome proliferator-activated receptors, Pathogenesis, Therapeutic strategies

摘要： 2型糖尿病（T2DM）常伴有代谢综合征的其他特征，会导致血管病变、终末期器官衰竭和癌症。代谢功能障碍相关脂肪性肝病（MASLD）是T2DM常见的并发症之一，超过70%的T2DM患者合并有MASLD。过氧化物酶体增殖激活受体（PPARs）参与脂肪酸吸收、β-氧化、脂肪生成、糖异生和胰岛素敏感性有关的基因表达。MASLD的发病机制与PPARs功能失调密切相关，其特征为脂肪酸氧化能力下降、脂肪组织功能紊乱，并伴随胰岛素敏感性降低及炎症信号通路异常激活。本篇综述旨在了解PPARs在T2DM合并MASLD中的重要机制与病理生理作用，为进一步研究PPARs靶向治疗T2DM合并MASLD提供理论依据。

关键词: 代谢功能障碍相关脂肪性肝病；糖尿病, 2 型；过氧化物酶体增殖物激活受体；发病机制；治疗策略