Insulin signaling, glucose metabolism, and the angiotensin II signaling system: studies in Bartter's/Gitelman's syndromes.
Insulin signaling, glucose metabolism, and the angiotensin II signaling system: studies in Bartter's/Gitelman's syndromes.
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胰岛素信号、葡萄糖代谢和血管紧张素 II 信号系统：巴特/吉特曼综合征的研究。
DOI：
10.2337/diacare.29.02.06.dc05-2048
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发表时间：
2006
期刊：
影响因子：
16.2
通讯作者：
L. Calò
中科院分区：
文献类型：
--
作者：
P. Davis;E. Pagnin;A. Semplicini;A. Avogaro;L. Calò
Taniyama等人（1）最近报道，血管紧张素II（Ang II）在体外通过Src、磷酸肌醇依赖性激酶-1和活性氧介导的Ser 307磷酸化降低胰岛素受体底物-1蛋白水平。这导致靶向胰岛素受体底物-1进行蛋白酶体依赖性降解，然后损害胰岛素信号传导。这些发现为了解血管紧张素Ⅱ 1型受体拮抗剂对胰岛素抵抗的积极作用的分子基础提供了理论依据。
血管紧张素II和胰岛素信号之间的关系显示在体外导致我们评估这是否也是在人体内运作。我们分析了一组患有Bartter/Gitelman综合征（BS/GS）的患者，尽管有高血压的典型生化和激素异常，但持续正常/低血压引起了广泛关注。BS/GS是由特定的肾脏转运蛋白和离子通道的基因缺陷引起的，表现为低钾血症、钠消耗、肾素-血管紧张素-醛固酮系统激活和高血压。
Taniyama et al. (1) have recently reported that angiotensin II (Ang II) in vitro decreases insulin receptor substrate-1 protein levels via Src, phosphoinositide-dependent kinase-1, and reactive oxygen species–mediated phosphorylation of Ser307. This leads to the targeting of insulin receptor substrate-1 for proteasome-dependent degradation, which then impairs insulin signaling. These findings provide a rationale for understanding the molecular basis of the positive effect of Ang II type 1 receptor antagonists on insulin resistance.
The relationship between Ang II and insulin signaling shown in vitro leads us to assess whether this is operative also in vivo in humans. We analyzed a cohort of patients with Bartter’s/Gitelman’s syndrome (BS/GS), which attract much attention for persistent normo-/hypotension despite biochemical and hormonal abnormalities typical of hypertension. BS/GS, caused by gene defects in specific kidney transporters and ion channels, presents hypokalemia, sodium depletion, activation of the renin-angiotensin-aldosterone system, and increased …
影响因子：
4.9
作者：
Mita, S;Kobayashi, N;Matsuoka, H
通讯作者：
Matsuoka, H