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首页> 外文期刊>Molecular and Cellular Biology >Disruption of the Selenocysteine Lyase-Mediated Selenium Recycling Pathway Leads to Metabolic Syndrome in Mice
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Disruption of the Selenocysteine Lyase-Mediated Selenium Recycling Pathway Leads to Metabolic Syndrome in Mice

机译：硒代半胱氨酸裂解酶介导的硒回收途径的破坏导致小鼠代谢综合症。

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Selenium (Se) is an essential trace element used for biosynthesis of selenoproteins and is acquired either through diet or cellular recycling mechanisms. Selenocysteine lyase (Scly) is the enzyme that supplies Se for selenoprotein biosynthesis via decomposition of the amino acid selenocysteine (Sec). Knockout (KO) of Scly in a mouse affected hepatic glucose and lipid homeostasis. Mice lacking Scly and raised on an Se-adequate diet exhibit hyperinsulinemia, hyperleptinemia, glucose intolerance, and hepatic steatosis, with increased hepatic oxidative stress, but maintain selenoprotein levels and circulating Se status. Insulin challenge of Scly KO mice results in attenuated Akt phosphorylation but does not decrease phosphorylation levels of AMP kinase alpha (AMPKα). Upon dietary Se restriction, Scly KO animals develop several characteristics of metabolic syndrome, such as obesity, fatty liver, and hypercholesterolemia, with aggravated hyperleptinemia, hyperinsulinemia, and glucose intolerance. Hepatic glutathione peroxidase 1 (GPx1) and selenoprotein S (SelS) production and circulating selenoprotein P (Sepp1) levels are significantly diminished. Scly disruption increases the levels of insulin-signaling inhibitor PTP1B. Our results suggest a dependence of glucose and lipid homeostasis on Scly activity. These findings connect Se and energy metabolism and demonstrate for the first time a unique physiological role of Scly in an animal model.
机译：硒（Se）是用于硒蛋白生物合成的必需微量元素，可通过饮食或细胞回收机制获得。硒代半胱氨酸裂解酶（Scly）是通过分解硒代半胱氨酸（Sec）而为硒提供硒蛋白生物合成酶。小鼠Scly的敲除（KO）影响了肝糖和脂质体内稳态。缺乏Scly并在硒充足的饮食中饲养的小鼠表现出高胰岛素血症，高瘦素血症，葡萄糖耐受不良和肝脂肪变性，肝脏氧化应激增加，但维持硒蛋白水平和循环性硒状态。 Scly KO小鼠的胰岛素攻击导致Akt磷酸化减弱，但不降低AMP激酶α（AMPKα）的磷酸化水平。限制饮食中的硒含量后，Scly KO动物会出现代谢综合征的一些特征，例如肥胖，脂肪肝和高胆固醇血症，并伴有高瘦素血症，高胰岛素血症和葡萄糖耐受不良。肝谷胱甘肽过氧化物酶1（GPx1）和硒蛋白S（SelS）的产生和循环硒蛋白P（Sepp1）的水平大大降低。 Scly破坏会增加胰岛素信号抑制剂PTP1B的水平。我们的结果表明葡萄糖和脂质稳态对Scly活性的依赖性。这些发现将硒与能量代谢联系起来，并首次证明了Scly在动物模型中的独特生理作用。

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