The failure of insulin to suppress glucose production by the liver is a key aspect of the insulin resistance seen in type 2 diabetes. Lipid-activated protein kinase C epsilon has long been identified as an important mediator of diet-induced glucose intolerance and hepatic insulin resistance and the current view emphasizes a mechanism involving phosphorylation of the insulin receptor by the kinase to inhibit downstream insulin action. However, the significance of this direct effect in the liver has now been challenged by tissue-specific deletion of PKCε, which demonstrated a more prominent role for the kinase in adipose tissue to promote glucose intolerance. New insights regarding the role of PKCε therefore contribute to the understanding of indirect effects on hepatic glucose metabolism.

中文翻译：

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解构 PKC Epsilon 在葡萄糖稳态中的作用

胰岛素不能抑制肝脏产生的葡萄糖是 2 型糖尿病胰岛素抵抗的一个关键方面。长期以来，脂质活化蛋白激酶 C epsilon 被认为是饮食诱导的葡萄糖耐受不良和肝脏胰岛素抵抗的重要介质，目前的观点强调了一种机制，该机制涉及激酶对胰岛素受体的磷酸化以抑制下游胰岛素作用。然而，这种直接作用在肝脏中的重要性现在受到 PKCε 的组织特异性缺失的挑战，这证明了激酶在脂肪组织中促进葡萄糖耐受不良的更突出作用。因此，关于 PKCε 作用的新见解有助于了解对肝葡萄糖代谢的间接影响。