Selenoprotein F knockout leads to glucose and lipid metabolism disorders in mice
Selenoprotein F knockout leads to glucose and lipid metabolism disorders in mice
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硒蛋白F敲除导致小鼠糖脂代谢紊乱
DOI：
10.1007/s00775-020-01821-z
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发表时间：
2020-09-29
影响因子：
3
通讯作者：
Huang, Kaixun
中科院分区：
文献类型：
--
作者：
Zheng, Xiaoxiang;Ren, Bingyu;Huang, Kaixun
硒蛋白F（Selenoprotein F，Selenof）是一种内质网（endoplasmic reticulum，ER）蛋白，被认为参与内质网中糖蛋白的折叠和质量控制。然而，其职能尚未得到彻底解决。在这项研究中，蛋白质组学分析表明，硒缺乏导致小鼠肝脏蛋白质的差异表达与葡萄糖和脂质代谢。表型分析显示，Selenof基因敲除小鼠即使在正常饮食下也表现出葡萄糖耐受不良和胰岛素减少。此外，Selenof基因敲除可加重高脂饮食诱导的肥胖、高血糖症、葡萄糖耐受不良和肝脂肪变性。此外，脂蛋白脂酶和羧酸酯酶1D，参与脂质代谢的两种糖蛋白，显着降低硒基因敲除小鼠的肝脏与正常或高脂饮食。总的来说，这些研究结果表明，硒缺乏可能会导致糖蛋白质量控制的扰动，从而有助于糖和脂质代谢紊乱，这意味着一个新的生物学功能的硒。
Selenoprotein F (Selenof), an endoplasmic reticulum (ER)-resident protein, is considered to be involved in glycoprotein folding and quality control in the ER. However, its function has not yet been thoroughly addressed. In this study, proteomics analysis revealed that Selenof deficiency in mice led to the differential expression of hepatic proteins associated with glucose and lipid metabolism. The phenotype analysis revealed that Selenof knockout mice showed glucose intolerance and insulin reduction, even with a normal diet. Additionally, Selenof knockout exacerbated high-fat diet-induced obesity, hyperglycemia, glucose intolerance, and hepatic steatosis. Furthermore, lipoprotein lipase and carboxylesterase 1D, two glycoproteins involved in lipid metabolism, were significantly decreased in the liver of Selenof knockout mice with a normal or high-fat diet. Collectively, these findings suggested that Selenof deficiency might cause the perturbation of glycoprotein quality control and thus contribute to glucose and lipid metabolism disorders, implying a novel biological function of Selenof.