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
Department of Medicine, Washington University School of Medicine, St. Louis, Missouri;
Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, Missouri;
Department of Medicine, Washington University School of Medicine, St. Louis, Missouri;
Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, Missouri;
Department of Medicine, University of Chicago, Chicago, Illinois;
Department of Medicine, University of Chicago, Chicago, Illinois;
Department of Medicine, Washington University School of Medicine, St. Louis, Missouri;
Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, Missouri;
Department of Medicine, Washington University School of Medicine, St. Louis, Missouri Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, Missouri;
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
机译:失活的β细胞ATP敏感性K(+)通道突变的载体具有正常的葡萄糖耐量和胰岛素敏感性以及适当的胰岛素分泌。
机译:Kir6.2的E23K变体与OGTT后血清胰岛素反应受损和2型糖尿病风险增加有关。
机译:胰岛素耐受性受损和空腹血糖诊断的胰岛素受体工作特征曲线分析
机译:偏心测力对绝经后糖耐量异常妇女胰岛素敏感性的影响。
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
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