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Kir6.2 Variant E23K Increases ATP-Sensitive K+ Channel Activity and Is Associated With Impaired Insulin Release and Enhanced Insulin Sensitivity in Adults With Normal Glucose Tolerance

机译:糖耐量正常的成年人,Kir6.2变异E23K增加ATP敏感性K +通道活性,并与胰岛素释放受损和胰岛素敏感性增强相关

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摘要

The E23K variant in the Kir6.2 subunit of the ATP-sensitive K(+) channel (K(ATP) channel) is associated with increased risk of type 2 diabetes. The present study was undertaken to increase our understanding of the mechanisms responsible. To avoid confounding effects of hyperglycemia, insulin secretion and action were studied in subjects with the variant who had normal glucose tolerance.
机译:ATP敏感性K(+)通道(K(ATP)通道)的Kir6.2亚基中的E23K变异与2型糖尿病的风险增加相关。进行本研究是为了增加我们对负责机制的了解。为了避免高血糖的混杂效应,对具有正常葡萄糖耐量的变异对象进行了胰岛素分泌和作用研究。

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  • 来源
    《Diabetes》 |2009年第8期|p.1869-1878|共10页
  • 作者单位

    Dennis T. Villareal,1 Joseph C. Koster,2 Heather Robertson,1 Alejandro Akrouh,2 Kazuaki Miyake,3 Graeme I. Bell,3 Bruce W. Patterson,1 Colin G. Nichols,2 and Kenneth S. Polonsky1,2From the 1 Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, the 2 Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, Missouri, and the 3 Department of Medicine. University of Chicago, Chicago, Illinois.Corresponding author: Kenneth S. Polonsky, polonsky@wustl.edu.Received 7 January 2009 and accepted 27 April 2009.Published ahead of print at http://diabetes.diabetesjom-nals.org on 2 June 2009. DOI: 10.2337/db09-0025.D.T.V. and J.CK. contributed equally to this research.© 2009 by die American Diabetes Associatioa Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/Ucenses/by -nc-nd/3.0/ for details.The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.,;

  • 收录信息 美国《科学引文索引》(SCI);美国《化学文摘》(CA);
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