Therapeutic potential of palmitoleic acid in non-alcoholic fatty liver disease: Targeting ferroptosis and lipid metabolism disorders

被引:4
|
作者
Wang, Hao [2 ]
Shan, Chunlan [3 ]
Guo, Gangjun [4 ]
Ning, Delu [1 ]
Miao, Fujun [1 ]
机构
[1] Yunnan Woody Oilseed Technol Innovat Ctr, Yunnan Acad Forestry & Grassland, Kunming 650204, Peoples R China
[2] Yunnan Agr Univ, Coll Food Sci & Technol, Kunming 650201, Peoples R China
[3] Guizhou Univ, Coll Anim Sci, Guiyang 550025, Peoples R China
[4] Yunnan Inst Trop Crops, Jinghong 666100, Peoples R China
关键词
Palmitoleic acid; Non-alcoholic fatty liver disease; Ferroptosis; Lipid metabolism; INSULIN-RESISTANCE; EXPRESSION;
D O I
10.1016/j.intimp.2024.113025
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Background: Non-alcoholic fatty liver disease (NAFLD) is a metabolic syndrome associated with obesity and type 2 diabetes mellitus. Currently, there are no effective drugs to treat NAFLD. Palmitoleic acid (PA) has demonstrated therapeutic potential in managing various metabolic diseases and inflammation. Although ferroptosis is known to play a critical role in the NAFLD development, it remains unclear whether PA can alleviate NAFLD by inhibiting ferroptosis. Methods: Thirty C57BL/6 mice were divided into three groups: standard diet, high-fat diet (HFD), and HFD with PA. The experiment lasted 16 weeks. Results: PA alleviated liver injury, hepatitis, and dyslipidemia in HFD-induced NAFLD mice. It improved insulin resistance, downregulated genes and proteins related to fat synthesis, and upregulated genes and proteins linked to lipolysis and fat oxidation. Mechanistically, bioinformatics enrichment revealed the involvement of ferroptosis in NAFLD. PA mitigated oxidative stress and reduced liver iron content in NAFLD. It downregulated acyl-CoA synthetase long-chain family member 4 (ACSL4) expression while upregulating glutathione peroxidase 4 (GPX4) and solute carrier family 7 member 11 (SLC7A11) expression, thereby inhibiting ferroptosis. Conclusion: PA exerts a protective effect against liver lipotoxicity by inhibiting lipid metabolism-mediated ferroptosis. These findings provide new insights into preventive and therapeutic strategies for the pathological processes of NAFLD.
引用
收藏
页数:12
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