Selenoprotein F (SELENOF)-mediated AKT1-FOXO3a-PYGL axis contributes to selenium supranutrition-induced glycogenolysis and lipogenesis
文献类型： 外文期刊
作者： Zhang, Dian-Guang 1 ; Zhao, Tao 1 ; Xu, Xiao-Jian 1 ; Xu, Yi-Huan 1 ; Wei, Xiao-Lei 1 ; Jiang, Ming 3 ; Luo, Zhi 1 ;
作者机构： 1.Huazhong Agr Univ, Fishery Coll, Key Lab Freshwater Anim Breeding, Minist Agr, Wuhan 430070, Peoples R China
2.Hubei Hongshan Lab, Wuhan 430070, Peoples R China
3.Chinese Acad Fishery Sci, Yangtze River Fisheries Res Inst, Fish Nutr & Feed Div, Wuhan 430223, Peoples R China
关键词： SELENOF; Lipid metabolism; AKT1-FOXO3a-PYGL axis; Glycogenolysis; Vertebrates
期刊名称：BIOCHIMICA ET BIOPHYSICA ACTA-GENE REGULATORY MECHANISMS （ 影响因子：6.304； 五年影响因子：5.214 ）
ISSN： 1874-9399
年卷期： 2022 年 1865 卷 3 期
页码：
收录情况： SCI
摘要： Mounting evidence showed that excess selenium (10.0-15.0-fold of adequate Se) intake caused severe hepatic lipid deposition in the vertebrate. However, the underlying mechanism remains unclear. The study was performed to elucidate the mechanism of Se supranutrition mediated-changes of lipid deposition and metabolism. We found that dietary excessive Se addition increased hepatic TGs and glucose contents, up-regulated lipogenic enzyme activities and reduced hepatic glycogen contents. Transcriptomic and immunoblotting analysis showed that Se supranutrition significantly influenced serine/threonine kinase 1 (AKT1)-forkhead box O3a (FOXO3a)-PYGL signaling and protein levels of SELENOF. Knockdown of SELENOF and PYGL by RNA interference revealed that the AKT1-FOXO3a-PYGL axis was critical for Se supranutrition-induced lipid accumulation. Moreover, Se supranutrition-induced lipid accumulation was via the increased DNA binding capacity of FOXO3a to PYGL promoter, which increased glycogenolysis, and accordingly promoted lipogenesis and lipid accumulation. Our finding provides new insight into the mechanism of Se supranutrition-induced lipid accumulation and suggests that SELENOF may be a therapeutic target for Se supranutrition induced-lipid disorders in the vertebrates.
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