Current Advances in the Regulatory Effects of Bioactive Compounds from Dietary Resources on Nonalcoholic Fatty Liver Disease: Role of Autophagy.
Yue ZhangQing ChenXiong FuSiming ZhuQiang HuangChao LiPublished in: Journal of agricultural and food chemistry (2023)
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.
Keyphrases
- oxidative stress
- signaling pathway
- diabetic rats
- cell death
- protein kinase
- transcription factor
- endoplasmic reticulum stress
- induced apoptosis
- insulin resistance
- dna damage
- ischemia reperfusion injury
- endoplasmic reticulum
- pi k akt
- type diabetes
- cell proliferation
- adipose tissue
- physical activity
- human health
- skeletal muscle
- epithelial mesenchymal transition
- dna binding
- fatty acid
- metabolic syndrome
- drug induced
- weight gain
- risk assessment
- stress induced
- polycystic ovary syndrome
- single cell
- body mass index