Review of Diabetes Mellitus Reduces the Function and Expression of Atp-Dependent K+ Channels in Cardiac Mitochondria

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Review of “Diabetes mellitus reduces the function and expression of ATP-dependent K+ channels in cardiac mitochondria” Ibra S. Fancher, Gregory M. Dick, John M. Hollander By: Cinthya Biochemistry Fall 2013 Abstract: The effect of type 1 diabetes on mitochondrial potassium sensitive channels (mitoKATP) in cardiac myocyte expression was studied in mice. The prediction was that mice who were randomly made hyperglycemic would have a reduction in their mitoKATP expression as well as a decrease in their diazoxide-induced depolarization (ΔΨm). MitoKATP were subcategorized as either in interfibrillar mitochondria (IFM or subsarcolemmal mitochondria (SSM). Male mice were assigned randomly to control (n=10) or diabetic groups (n=10). The diabetic group was made hyperglycemic via IP injection of streptozotocin and after 5weeks of measuring blood glucose levels>250mg/dL to confirm hyperglycemia. MitoKATP expression was determined via Western blot analysis and ΔΨm was measured with the potentiometric dye rhodamine 123. Diabetes reduced Kir6.1 and SUR1 expression in IFM by over 40% (p<0.05) as well as KIR6.1 in SSM by around 40% (p<0.05). Conversely, SUR1 expression was not impacted by diabetes (p>0.05). Opening mitoKATP with diazoxide depolarized the control IFM ΔΨm by 80% compare to the diabetic IFM depolarization of only 30% (p<0.05). Diazoxide induced depolarization was not affected by diabetes (20-30%). The data is indicative that diabetes reduces mitoKATP expression and function in IFM and can help and provide an opportunity to understand more about diabetic cardiomyopathy and the loss of cardioprotective mechanisms in the diabetic heart. Introduction: Individuals with type 1 diabetes suffer from a complete lack of or little production of insulin from beta cells in the pancreas. The lack of insulin results in the difficulty in metabolic

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