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Oxidative stress and beta-cell dysfunction
Observations are of great importance for clinical intervention because they show a possibility to protect beta-cells at an early stage before dramatic changes of the secretory capacity and loss of cell mass become manifest and lead to glucose intolerance or even overt diabetes. Expand
Electrophysiology of islet cells.
Stimulus-Secretion Coupling (SSC) of pancreatic islet cells comprises electrical activity. Changes of the membrane potential (V(m)) are regulated by metabolism-dependent alterations in ion channelExpand
Parallel oscillations of intracellular calcium activity and mitochondrial membrane potential in mouse pancreatic B-cells.
Glucose metabolism via mitochondrial ATP production and closure of K(+)(ATP) channels induces an increase in [Ca(2+)](c), which in turn decreases ATP synthesis by depolarizing DeltaPsi, thus transiently terminating Ca(2+) influx. Expand
ABCC8 and ABCC9: ABC transporters that regulate K+ channels
Studies on KATP channel null mice are clarifying the roles of these metabolically sensitive channels in a variety of tissues, including endocrine cells, neurons, and both smooth and striated muscle. Expand
Elevated Blood Pressure Linked to Primary Hyperaldosteronism and Impaired Vasodilation in BK Channel–Deficient Mice
It is reported that deletion of the pore-forming BK channel &agr; subunit leads to a significant blood pressure elevation resulting from hyperaldosteronism accompanied by decreased serum K+ levels as well as increased vascular tone in small arteries. Expand
Interference of H2O2 with stimulus‐secretion coupling in mouse pancreatic β‐cells
It is demonstrated that H2O2 interferes with glucose metabolism, which influences the membrane potential and ATP‐sensitive K+ current via the intracellular concentration of ATP, which leads to an inhibition of insulin secretion despite an increase in [Ca2+]i. Expand
Suppression of KATP channel activity protects murine pancreatic beta cells against oxidative stress.
Sur1-/- mice were less susceptible than WT mice to streptozotocin-induced beta cell destruction and subsequent hyperglycemia and death, which suggests that loss of KATP channel activity may protect against streptozootocIn-induced diabetes in vivo. Expand
Ion channels involved in insulin release are activated by osmotic swelling of pancreatic B-cells.
The results suggest that regulatory volume decrease is achieved by activation of K+ and Cl- currents, which is responsible for the previously described depolarization and increase in insulin release induced by osmotic cell swelling. Expand
An adenylate kinase is involved in KATP channel regulation of mouse pancreatic beta cells
It is proposed that phosphotransfer events mediated by AK and CK play an important role in determining the effective concentrations of ATP and ADP in the microenvironment of pancreatic beta cell KATP channels. Expand
Effects of the Nitric Oxide Synthase Inhibitor NωNitro-l-arginine Methyl Ester on Electrical Activity and Ion Channels of Mouse Pancreatic B Cells
Abstract The effects of the nitric oxide (NO) synthase inhibitor N ω -nitro-L-arginine methyl ester (L-NAME) were studied on electrical activity, K + ATP currents and voltage-dependent K + and Ca 2+Expand