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Novel insights into pancreatic β-cell glucolipotoxicity from real-time functional analysis of mitochondrial energy metabolism in INS-1E insulinoma cells.
High circulating glucose and non-esterified (free) fatty acid levels can cause pancreatic β-cell failure. The molecular mechanisms of this β-cell glucolipotoxicity are yet to be established conclusively. In the present ...
Insulin acutely improves mitochondrial function of rat and human skeletal muscle by increasing coupling efficiency of oxidative phosphorylation.
Insulin is essential for the regulation of fuel metabolism and triggers the uptake of glucose by skeletal muscle. The imported glucose is either stored or broken down, as insulin stimulates glycogenesis and ATP synthesis. ...
Mitochondrialuncouplingprotein-2isnotinvolvedin palmitate-induced impairmentofglucose-stimulatedinsulinsecretion in INS-1Einsulinomacellsandisnotneededfortheamplification of insulin release
WehaverecentlyshownthatovernightexposureofINS-1Einsulinomacellstopalmitateinthepresence of highglucosecausesdefectsinbothmitochondrialenergymetabolismandglucose-stimulatedinsulin secretion (GSIS).Herewereportexperimentsd ...
Uncoupling protein-2 attenuates palmitoleate protection against the cytotoxic production of mitochondrial reactive oxygen species in INS-1E insulinoma cells.
High glucose and fatty acid levels impair pancreatic beta cell function. We have recently shown that palmitate-induced loss of INS-1E insulinoma cells is related to increased reactive oxygen species (ROS) production as ...
Energization-dependent endogenous activation of proton conductance in skeletal muscle mitochondria.
Leak of protons into the mitochondrial matrix during substrate oxidation partially uncouples electron transport from phosphorylation of ADP, but the functions and source of basal and inducible proton leak in vivo remain ...