Reactive oxygen species enhance insulin sensitivity.
Reactive oxygen species enhance insulin sensitivity.
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DOI：
10.1016/j.cmet.2009.08.009
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发表时间：
2009-10
期刊：
影响因子：
29
通讯作者：
Tiganis T
中科院分区：
文献类型：
--
作者：
Loh K;Deng H;Fukushima A;Cai X;Boivin B;Galic S;Bruce C;Shields BJ;Skiba B;Ooms LM;Stepto N;Wu B;Mitchell CA;Tonks NK;Watt MJ;Febbraio MA;Crack PJ;Andrikopoulos S;Tiganis T
线粒体产生的慢性活性氧（ROS）可能有助于胰岛素抵抗的发展，这是2型糖尿病的主要特征。近年来，对胰岛素等生理刺激产生的ROS也可能通过可逆氧化和抑制蛋白酪氨酸磷酸酶（PTPs）促进信号传导。在这里，我们报道缺乏参与消除生理性ROS的关键酶之一的小鼠，谷胱甘肽过氧化物酶1 (Gpx1)，可以保护小鼠免受高脂肪饮食诱导的胰岛素抵抗。Gpx1−/−小鼠的胰岛素敏感性增加归因于胰岛素诱导的磷脂酰肌醇-3-激酶/Akt信号和肌肉中的葡萄糖摄取，并且可以通过抗氧化剂n-乙酰半胱氨酸逆转。胰岛素信号的增加与PTP家族成员PTEN的氧化增强相关，PTEN会终止磷脂酰肌醇-3激酶产生的信号。这些研究为体内ROS增强胰岛素信号提供了因果证据。
Chronic reactive oxygen species (ROS) production by mitochondria may contribute to the development of insulin resistance, a primary feature of type 2 diabetes. In recent years it has become apparent that ROS generation in response to physiological stimuli such as insulin may also facilitate signaling by reversibly oxidizing and inhibiting protein tyrosine phosphatases (PTPs). Here we report that mice lacking one of the key enzymes involved in the elimination of physiological ROS, glutathione peroxidase 1 (Gpx1), were protected from high fat diet-induced insulin resistance. The increased insulin sensitivity in Gpx1−/− mice was attributed to insulin-induced phosphatidylinositol-3-kinase/Akt signaling and glucose uptake in muscle and could be reversed by the anti-oxidant N-acetylcysteine. Increased insulin signaling correlated with enhanced oxidation of the PTP family member PTEN, which terminates signals generated by phosphatidylinositol-3-kinase. These studies provide causal evidence for the enhancement of insulin signaling by ROS in vivo.
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DOI：
10.1152/ajpendo.00461.2003
发表时间：
2004-07-01
影响因子：
5.1
作者：
Lee, FN;Zhang, LH;Youn, JH
通讯作者：
Youn, JH
影响因子：
4.8
作者：
Lee, SR;Yang, KS;Rhee, SG
通讯作者：
Rhee, SG
DOI：
10.1073/pnas.0804336105
发表时间：
2008-07-22
影响因子：
11.1
作者：
Boivin, Benoit;Zhangt, Sheng;Tonks, Nicholas K.
通讯作者：
Tonks, Nicholas K.
影响因子：
29
作者：
Cho, Charles Y.;Koo, Seung-Hoi;Chanda, Surnit K.
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Chanda, Surnit K.
影响因子：
15.9
作者：
Anderson, Ethan J.;Lustig, Mary E.;Neufer, P. Darrell
通讯作者：
Neufer, P. Darrell