4.5 Article

Ablation of fatty acid desaturase 2 (FADS2) exacerbates hepatic triacylglycerol and cholesterol accumulation in polyunsaturated fatty acid-depleted mice

期刊

FEBS LETTERS
卷 595, 期 14, 页码 1920-1932

出版社

WILEY
DOI: 10.1002/1873-3468.14134

关键词

cholesterol; fatty acid desaturase; hepatic steatosis; highly unsaturated fatty acids; lipogenesis; polyunsaturated fatty acid

资金

  1. Ministry of Education, Culture, Sports, Science and Technology (MEXT)/Japanese Society for the Promotion of Sport [17K00848, 20K02383, 15H06600, 18K16246, 21K08565]
  2. Mishima Kaiun Memorial Foundation
  3. Takeda Science Foundation
  4. Grants-in-Aid for Scientific Research [21K08565, 20K02383, 17K00848, 18K16246, 15H06600] Funding Source: KAKEN

向作者/读者索取更多资源

This study found that >= C20 PUFAs synthesized by FADS2 are crucial in regulating hepatic triacylglycerol and cholesterol accumulation during PUFA deficiency.
Deficiency of polyunsaturated fatty acids (PUFAs) is known to induce hepatic steatosis. However, it is not clearly understood which type of PUFA is responsible for the worsening of steatosis. This study observed a marked accumulation of hepatic triacylglycerol and cholesterol in fatty acid desaturase 2 knockout (FADS2(-/-)) mice lacking both C18 and >= C20 PUFAs that were fed a PUFA-depleted diet. Hepatic triacylglycerol accumulation was associated with enhanced sterol regulatory element-binding protein (SREBP)-1-dependent lipogenesis and decreased triacylglycerol secretion into the plasma via very-low-density lipoprotein (VLDL). Furthermore, upregulation of cholesterol synthesis contributed to increased hepatic cholesterol content in FADS2(-/-) mice. These results suggest that >= C20 PUFAs synthesized by FADS2 are important in regulating hepatic triacylglycerol and cholesterol accumulation during PUFA deficiency.

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