Current Advances in the Regulatory Effects of Bioactive Compounds from Dietary Resources on Nonalcoholic Fatty Liver Disease: Role of Autophagy

自噬 非酒精性脂肪肝 雷帕霉素的作用靶点 安普克 脂肪肝 生物 胰岛素抵抗 过氧化物酶体 脂质代谢 药理学 蛋白激酶A 医学 内科学 生物化学 内分泌学 激酶 疾病 糖尿病 受体 细胞凋亡
作者
Yue Zhang,Qing Chen,Xiong Fu,Siming Zhu,Qiang Huang,Chao Li
出处
期刊:Journal of Agricultural and Food Chemistry [American Chemical Society]
卷期号:71 (46): 17554-17569 被引量:1
标识
DOI:10.1021/acs.jafc.3c04692
摘要

Nonalcoholic fatty liver disease (NAFLD) is the most prevalent chronic liver disease characterized by lipid metabolic disorder primarily due to sedentary lifestyles and excessive food consumption. However, there are currently no approved and effective drugs available to treat NAFLD. In recent years, research has shown that dietary bioactive compounds, such as polysaccharides, polyphenols, flavones, and alkaloids, have the potential to improve NAFLD by regulating autophagy. However, there is no up-to-date review of research progress in this field. This review aims to systematically summarize and discuss the regulatory effects and molecular mechanisms of dietary bioactive compounds on NAFLD through the modulation of autophagy. The existing research has demonstrated that some dietary bioactive compounds can effectively improve various aspects of NAFLD progression, such as lipid metabolism, insulin resistance (IR), endoplasmic reticulum (ER) stress, oxidative stress, mitochondrial homeostasis, and inflammation. Molecular mechanism studies have revealed that they exert their beneficial effects on NAFLD through autophagy-mediated signaling pathways, predominantly involving transcription factor EB (TFEB), mammalian target of rapamycin (mTOR), adenosine monophosphate-activated protein kinase (AMPK), peroxisome proliferator-activated receptors (PPARs), SIRT, and PTEN-induced kinase 1 (PINK1)/parkin. Furthermore, the challenges and prospects of current research in this field are highlighted. Overall, this review provides valuable insights into the potential treatment of NAFLD using dietary bioactive compounds that can modulate autophagy.
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