Pea Albumin Extracted from Pea ( Pisum sativum L.) Seeds Ameliorates High-Fat-Diet-Induced Non-Alcoholic Fatty Liver Disease by Regulating Lipogenesis and Lipolysis Pathways.
Shucheng ZhangZhengwu CuiHao ZhangPeng-Jie WangFuqing WangJian ZhangPublished in: Nutrients (2024)
Non-alcoholic fatty liver disease (NAFLD) is now recognized as the most prevalent liver disease globally. Pea albumin (PA) has demonstrated positive impacts on reducing obesity and improving glucose metabolism. In this research, a mouse model of NAFLD induced by a high-fat diet (HFD) was employed to examine the impact of PA on NAFLD and explore its potential mechanisms. The findings revealed that mice subjected to a HFD developed pronounced fatty liver alterations. The intervention with PA significantly lowered serum TC by 26.81%, TG by 43.55%, and LDL-C by 57.79%. It also elevated HDL-C levels by 1.2 fold and reduced serum ALT by 37.94% and AST by 31.21% in mice fed a HFD. These changes contributed to the reduction in hepatic steatosis and lipid accumulation. Additionally, PA improved insulin resistance and inhibited hepatic oxidative stress and inflammatory responses. Mechanistic studies revealed that PA alleviated lipid accumulation in HFD-induced NAFLD by activating the phosphorylation of AMPKα and ACC, inhibiting the expression of SREBF1 and FASN to reduce hepatic lipogenesis, and increasing the expression of ATGL, PPARα, and PPARγ to promote lipolysis and fatty acid oxidation. These results indicate that PA could serve as a dietary supplement for alleviating NAFLD, offering a theoretical foundation for the rational intake of PA in NAFLD intervention.
Keyphrases
- insulin resistance
- high fat diet induced
- high fat diet
- adipose tissue
- skeletal muscle
- metabolic syndrome
- polycystic ovary syndrome
- type diabetes
- mouse model
- randomized controlled trial
- oxidative stress
- fatty acid
- poor prognosis
- signaling pathway
- glycemic control
- dna damage
- liver fibrosis
- diabetic rats
- body mass index
- physical activity
- high glucose
- single cell
- nitric oxide
- binding protein
- induced apoptosis
- low density lipoprotein