Pea Albumin Alleviates Oleic Acid-Induced Lipid Accumulation in LO2 Cells Through Modulating Lipid Metabolism and Fatty Acid Oxidation Pathways
- Bing Fang 1,2, Jie Luo 3, Zhengwu Cui 1, Rong Liu 1, Pengjie Wang 1,2, Jian Zhang 1
- Bing Fang 1,2, Jie Luo 3, Zhengwu Cui 1
- 1Department of Nutrition and Health, China Agricultural University, Beijing 100193, China.
- 2Food Laboratory of Zhongyuan, Luohe 462300, China.
- 3College of Food Science and Technology, Hunan Agricultural University, Changsha 410114, China.
- 0Department of Nutrition and Health, China Agricultural University, Beijing 100193, China.
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View abstract on PubMed
Summary
This summary is machine-generated.Pea protein (PA) effectively reduces liver fat accumulation in a cell model of non-alcoholic fatty liver disease (NAFLD). It works by improving lipid metabolism and reducing cellular damage and oxidative stress.
Area Of Science
- Biochemistry
- Cell Biology
- Nutritional Science
Background
- Non-alcoholic fatty liver disease (NAFLD) is characterized by excessive lipid accumulation in the liver, potentially leading to chronic liver injury.
- Dietary proteins are being investigated for their potential to mitigate liver lipid accumulation.
Purpose Of The Study
- To investigate the mechanism by which pea albumin (PA) regulates lipid levels in vitro using a stable oleic acid (OA)-induced LO2 cell lipid accumulation model.
- To explore PA's effects on OA-induced cellular damage and oxidative stress.
Main Methods
- Established a stable in vitro LO2 cell model of lipid accumulation induced by oleic acid (OA).
- Assessed the impact of pea albumin (PA) on intracellular lipid droplet aggregation, triglyceride (TG), and total cholesterol (TC) levels.
- Evaluated PA's effects on cell viability, oxidative stress markers (MDA, GSH-Px), and liver enzyme secretion (ALT, AST).
- Analyzed the regulation of lipid metabolism pathways, including lipid synthesis, triglyceride catabolism, and fatty acid oxidation.
Main Results
- Pea albumin (PA) ameliorated OA-induced lipid accumulation in LO2 cells, reducing intracellular lipid droplets and lowering TG and TC levels.
- PA alleviated OA-induced cellular damage and oxidative stress, decreasing ALT, AST, and MDA levels while increasing GSH-Px viability.
- PA regulated lipid metabolism by inhibiting the lipid synthesis pathway and activating triglyceride catabolic and fatty acid oxidation pathways.
Conclusions
- Pea albumin (PA) effectively regulates lipid accumulation in LO2 cells, offering a potential dietary strategy for managing NAFLD.
- This study provides novel insights into the mechanism of protein-mediated regulation of liver cell lipid metabolism, supporting PA as a therapeutic agent.
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