Kurzfassung

ATP-sensitive potassium (KATP) channels of the ‘pancreatic’ type, i.e. containing the subunits SUR1 and Kir6.2, occur in ventricular myocytes, where they are stored in the Golgi complex to enable signal-transduction dependent translocation to the cell surface. We have recently shown that beta-adrenergic stimulation can deploy these channels. Based on recent reports that leptin signaling increases the plasma membrane localization of SUR1/Kir6.2-containing KATP channels in pancreatic beta cells...ATP-sensitive potassium (KATP) channels of the ‘pancreatic’ type, i.e. containing the subunits SUR1 and Kir6.2, occur in ventricular myocytes, where they are stored in the Golgi complex to enable signal-transduction dependent translocation to the cell surface. We have recently shown that beta-adrenergic stimulation can deploy these channels. Based on recent reports that leptin signaling increases the plasma membrane localization of SUR1/Kir6.2-containing KATP channels in pancreatic beta cells we aim to test whether leptin signaling also affects KATP channels present in cardiomyocytes. We expect unifying insights into the physiological regulation of an important ion channel and into the impact of the obese state on cardiac KATP channels. These results will contribute to ongoing discussions whether drugs targeting KATP channels may increase the cardiovascular risk of type II diabetic patients, which are often obese.
The cooperation between the Schwappach laboratory with long-standing expertise in KATP channel cell biology and biochemistry and the Schäfer laboratory with extensive expertise in leptin signaling in the cardiovascular system is key to tackling this problem. Only the collaborative effort can cover the required methodological spectrum and the student involved will strongly benefit from expert supervision in both areas.» weiterlesen» einklappen