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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
Dexamethasone Induces Cell Death in Insulin-Secreting Cells, an Effect Reversed by Exendin-4
In conclusion, glucocorticoid-induced apoptosis in insulin-secreting cells is accompanied by a downregulation of Bcl-2, activation of calcineurin with subsequent dephosphorylation of BAD, and mitochondrial depolarization. Expand
Mechanisms of the stimulation of insulin release by arginine-vasopressin in normal mouse islets.
AVP is not an initiator of insulin release, but it potently amplifies glucose-induced insulin release in normal mouse B-cells, which involves a stimulation of phosphoinositide metabolism, and presumably an activation of protein kinase C, rather than a change in cAMP levels or a direct control of the membrane potential. 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
The Gq/G11-mediated signaling pathway is critical for autocrine potentiation of insulin secretion in mice.
The Gq/G11-mediated signaling pathway potentiates insulin secretion in response to glucose by integrating systemic as well as autocrine/paracrine mediators. Expand