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首页> 外文期刊>Cell metabolism >Specific roles of the p110alpha isoform of phosphatidylinsositol 3-kinase in hepatic insulin signaling and metabolic regulation.
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Specific roles of the p110alpha isoform of phosphatidylinsositol 3-kinase in hepatic insulin signaling and metabolic regulation.

机译：磷脂酰肌醇3-激酶的p110alpha亚型在肝胰岛素信号传导和代谢调节中的特定作用。

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摘要

The class I(A) phosphatidylinsositol 3-kinases (PI3Ks) form a critical node in the insulin metabolic pathway; however, the precise roles of the different isoforms of this enzyme remain elusive. Using tissue-specific gene inactivation, we demonstrate that p110alpha catalytic subunit of PI3K is a key mediator of insulin metabolic actions in the liver. Thus, deletion of p110alpha in liver results in markedly blunted insulin signaling with decreased generation of PIP(3) and loss of insulin activation of Akt, defects that could not be rescued by overexpression of p110beta. As a result, mice with hepatic knockout of p110alpha display reduced insulin sensitivity, impaired glucose tolerance, and increased gluconeogenesis, hypolipidemia, and hyperleptinemia. The diabetic syndrome induced by loss of p110alpha in liver did not respond to metformin treatment. Together, these data indicate that the p110alpha isoform of PI3K plays a fundamental role in insulin signaling and control of hepatic glucose and lipid metabolism.
机译：I（A）类磷脂酰肌醇3激酶（PI3K）在胰岛素代谢途径中形成关键节点;然而，该酶不同同工型的确切作用仍然难以捉摸。使用组织特异性基因失活，我们证明PI3K的p110alpha催化亚基是肝脏中胰岛素代谢作用的关键介质。因此，肝脏中p110alpha的缺失导致胰岛素信号明显减弱，PIP（3）的生成减少，Akt的胰岛素激活丧失，p110beta的过表达无法挽救这些缺陷。结果，具有肝敲除p110alpha的小鼠表现出降低的胰岛素敏感性，受损的糖耐量和增加的糖异生，低脂血症和高瘦素血症。肝中p110alpha缺失引起的糖尿病综合征对二甲双胍治疗无反应。总之，这些数据表明PI3K的p110alpha同工型在胰岛素信号传导和肝葡萄糖和脂质代谢的控制中起着基本作用。

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