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Deficiency of IRTKS as an adaptor of insulin receptor leads to insulin resistance
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Deficiency of IRTKS as an adaptor of insulin receptor leads to insulin resistance
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Journal Article
Deficiency of IRTKS as an adaptor of insulin receptor leads to insulin resistance
2013
Overview
IRTKS encodes a member of the IRSp53/MIM homology domain family, which has been shown to play an im- portant role in the formation of plasma membrane protrusions. Although the phosphorylation of IRTKS occurs in response to insulin stimulation, the role of this protein in insulin signaling remains unknown. Here we show that IRTKS-deficient mice exhibit insulin resistance, including hyperglycemia, hyperinsulinemia, glucose intolerance, de- creased insulin sensitivity, and increased hepatic glucose production. The administration of ectopic IRTKS can ame- liorate the insulin resistance of IRTKS-deficient and diabetic mice. In parallel, the expression level of IRTKS was sig- nificantly decreased in diabetic mouse model. Furthermore, DNA hypermethylation of the IRTKS promoter was also observed in these subjects. We also show that IRTKS, as an adaptor of the insulin receptor （IR）, modulates IR-IRSI- PI3K-AKT signaling via regulating the phosphorylation of IR. These findings add new insights into our understand- ing of insulin signaling and resistance.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ Animals
/ Biomedical and Life Sciences
/ DNA
/ Mice
/ Microfilament Proteins - deficiency
/ Original
/ Receptor, Insulin - metabolism
/ 信号传导
/ 同源结构域
/ 小鼠模型
/ 磷酸化
/ 胰岛素受体
/ 胰岛素抵抗
/ 葡萄糖
/ 适配器
