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首页> 外文期刊>Life sciences >Diabetes mellitus reduces the function and expression of ATP-dependent K+ channels in cardiac mitochondria
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Diabetes mellitus reduces the function and expression of ATP-dependent K+ channels in cardiac mitochondria

机译：糖尿病减少了心脏线粒体中ATP依赖性K +通道的功能和表达

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Aim Our goal was to determine the effects of type I diabetes mellitus on the function and expression of ATP-dependent K+ channels in cardiac mitochondria (mitoKATP), composed of a pore-forming subunit (Kir6.1) and a diazoxide-sensitive sulphonylurea receptor (SUR1). We tested the hypothesis that diabetes reduces Kir6.1 and SUR1 expression as well as diazoxide-induced depolarization of mitochondrial membrane potential (????m). Main methods Male FVB mice were made diabetic for 5 weeks with multiple low dose injections of streptozotocin. Cardiac mitochondria were separated into two populations: subsarcolemmal mitochondria (SSM) and interfibrillar mitochondria (IFM). mitoKATP expression was determined via Western blot analysis of Kir6.1 and SUR1 proteins. mitoKATP function was determined by measuring ????m with the potentiometric dye rhodamine 123. Key findings Diabetes reduced Kir6.1 and SUR1 expression in IFM by over 40% (p 0.05 for both). Similarly, diabetes reduced Kir6.1 expression in SSM by approximately 40% (p 0.05); however, SUR1 expression was unaffected. Opening mitoKATP with diazoxide (100 ??M) depolarized control IFM ????m by 80% of the valinomycin maximum; diabetic IFM depolarized only 30% (p 0.05). Diazoxide-induced depolarization was much less in SSM (20-30%) and unaffected by diabetes. Significance Our data indicate that diabetes reduces mitoKATP expression and function in IFM. These changes in mitoKATP may provide an opportunity to understand mechanisms leading to diabetic cardiomyopathy and loss of cardioprotective mechanisms in the diabetic heart. ? 2013 Elsevier Inc.
机译：目的我们的目标是确定I型糖尿病患者对心脏线粒体（MITOKATP）中ATP依赖性K +通道的功能和表达的影响，由孔形成亚基（KIR6.1）和一种二氮氧化物敏感的磺酰脲受体组成（ur1）。我们测试了糖尿病减少kir6.1和sur1表达以及二边氧化物诱导的线粒体膜电位的去极化的假设（???? m）。主要方法雄性FVB小鼠进行糖尿病5周，具有多种低剂量注射链脲佐菌素。心脏线粒体分为两种群体：子芦荟线粒体（SSM）和Interfibrillar Mitochondria（IFM）。通过KIR6.1和SUR1蛋白的蛋白质印迹分析测定MITOKATP表达。 MITOKATP功能是通过测量电位染料罗丹明123的测量来确定的。关键发现糖尿病将KIR6.1和IFM中的SUR1表达减少超过40％（对两者为0.05）。类似地，糖尿病将Kir6.1在SSM中的表达降低约40％（P <0.05）;然而，SUR1表达不受影响。用二氮杂化（100→M）去极化控制IFM的MITOKATP（100→M）达到80％的缬氨酸霉素最大值;糖尿病IFM仅取代30％（P <0.05）。 SSM（20-30％）的二氮杂氧基诱导的去极化较少，并未受糖尿病影响。重要性我们的数据表明糖尿病在IFM中降低了MITOKATP表达和功能。 MITOKATP的这些变化可以提供理解导致糖尿病心脏病和糖尿病心脏心脏保护机制丧失机制的机制。还是2013年elsevier公司

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