PDF(Pubmed)
Abstract：
The global prevalence of Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) is increasing, now affecting 25%-30% of the population worldwide. MASLD, characterized by hepatic steatosis, results from an imbalance in lipid metabolism, leading to oxidative stress, lipoperoxidation, and inflammation. The activation of autophagy, particularly lipophagy, alleviates hepatic steatosis by regulating intracellular lipid levels. Lutein, a carotenoid with antioxidant and anti-inflammatory properties, protects against liver damage, and individuals who consume high amounts of lutein have a lower risk of developing MASLD. Evidence suggests that lutein could modulate autophagy-related signaling pathways, such as the transcription factor EB (TFEB). TFEB plays a crucial role in regulating lipid homeostasis by linking autophagy to energy metabolism at the transcriptional level, making TFEB a potential target against MASLD. STARD3, a transmembrane protein that binds and transports cholesterol and sphingosine from lysosomes to the endoplasmic reticulum and mitochondria, has been shown to transport and bind lutein with high affinity. This protein may play a crucial role in the uptake and transport of lutein in the liver, contributing to the decrease in hepatic steatosis and the regulation of oxidative stress and inflammation. This review summarizes current knowledge on the role of lutein in lipophagy, the pathways it is involved in, its relationship with STARD3, and its potential as a pharmacological strategy to treat hepatic steatosis.
摘要：
代谢功能障碍相关的脂肪性肝病（MASLD）的全球患病率正在增加，现在影响了全世界25%-30%的人口。MASLD,以肝脏脂肪变性为特征，脂质代谢失衡的结果，导致氧化应激，脂过氧化,和炎症。自噬的激活，特别是吸脂症，通过调节细胞内脂质水平减轻肝脏脂肪变性。叶黄素,具有抗氧化和抗炎特性的类胡萝卜素，防止肝脏损伤，消耗大量叶黄素的人患MASLD的风险较低。有证据表明，叶黄素可以调节自噬相关的信号通路，例如转录因子EB(TFEB)。TFEB通过在转录水平将自噬与能量代谢联系起来，在调节脂质稳态中起着至关重要的作用，使TFEB成为对抗MASLD的潜在靶标。STARD3，一种跨膜蛋白，结合胆固醇和鞘氨醇并将其从溶酶体转运至内质网和线粒体，已显示具有高亲和力的运输和结合叶黄素。这种蛋白质可能在肝脏中叶黄素的摄取和运输中起关键作用，有助于减少肝脏脂肪变性和调节氧化应激和炎症。这篇综述总结了目前关于叶黄素在吸脂症中的作用的知识。它所涉及的途径，它与STARD3的关系，以及它作为治疗肝性脂肪变性的药理学策略的潜力。
