Insulin resistance and a diabetes mellitus-like syndrome in mice lacking the protein kinase Akt2 (PKBβ)
Insulin resistance and a diabetes mellitus-like syndrome in mice lacking the protein kinase Akt2 (PKBβ)
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DOI：
10.1126/science.292.5522.1728
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发表时间：
2001-06-01
期刊：
影响因子：
56.9
通讯作者：
Birnbaum, MJ
中科院分区：
文献类型：
--
作者：
Cho, H;Mu, J;Birnbaum, MJ
葡萄糖稳态取决于靶组织（最为重要的是肌肉和肝脏）对胰岛素的反应性。胰岛素作用的关键起始步骤包括支架蛋白的磷酸化以及磷脂酰肌醇3 - 激酶的激活。这些早期事件导致丝氨酸 - 苏氨酸蛋白激酶Akt（也称为蛋白激酶B）的激活。我们发现，Akt2基因缺陷的小鼠由于胰岛素对肝脏和骨骼肌作用存在缺陷，其胰岛素降低血糖的能力受损。这些数据表明Akt2是维持正常葡萄糖稳态的一个必需基因。
Glucose homeostasis depends on insulin responsiveness in target tissues, most importantly, muscle and Liver. The critical initial steps in insulin action include phosphorylation of scaffolding proteins and activation of phosphatidylinositol 3-kinase. These early events Lead to activation of the serine-threonine protein kinase Akt, also known as protein kinase B. We show that mice deficient in Akt2 are impaired in the ability of insulin to Lower blood glucose because of defects in the action of the hormone on Liver and skeletal muscle. These data establish Akt2 as an essential gene in the maintenance of normal glucose homeostasis.