n-3 Polyunsaturated fatty acid attenuates hyperhomocysteinemia-induced hepatic steatosis by increasing hepatic LXA
- Author:
Hao SONG
1
;
Jin-Jie DUAN
1
;
Kan LI
1
;
Liu YAO
2
;
Yi ZHU
1
Author Information
1. Department of Physiology and Pathophysiology, Tianjin Medical University, Tianjin 300070, China.
2. Department of Physiology and Pathophysiology, Tianjin Medical University, Tianjin 300070, China. yaoliu@tmu.edu.cn.
- Publication Type:Journal Article
- MeSH:
Animals;
Fatty Acids, Omega-3;
Fatty Liver/drug therapy*;
Hyperhomocysteinemia/drug therapy*;
Liver;
Male;
Mice;
Mice, Inbred C57BL
- From:
Acta Physiologica Sinica
2021;73(4):551-558
- CountryChina
- Language:Chinese
-
Abstract:
Nonalcoholic fatty liver disease (NAFLD) and hyperhomocysteinemia (HHcy) both are major health problems worldwide, whose incidence are closely related with each other. We previously reported the mechanism of HHcy-caused hepatic steatosis, but the role of n-3 polyunsaturated fatty acid (n-3 PUFA) in HHcy-induced hepatic steatosis remains unclear. In this study, 6-week-old C57BL/6 male mice were given a high methionine diet (HMD, 2% methionine diet), and plasma homocysteine levels were measured by ELISA to confirm the establishment of an HHcy model. Meantime, mice were fed HMD with or without n-3 PUFA supplement for 8 weeks to determine the role and mechanism of n-3 PUFA in hepatic steatosis induced by HHcy. Results showed that n-3 PUFA significantly improved hepatic lipid deposition induced by HHcy. qRT-PCR analysis demonstrated that n-3 PUFA inhibited the upregulation of Cd36, a key enzyme of fatty acid uptake, caused by HHcy. Further, the inhibition of hepatic Cd36 expression was associated with the inactivation of aryl hydrocarbon receptor (Ahr) induced by n-3 PUFA. Of note, mass spectrometry revealed that hepatic content of lipoxin A
