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Initiation and execution of lipotoxic ER stress in pancreatic β-cells
TLDR
Saturated FFA induce ER stress via ER Ca2+ depletion and the IRE1 and resulting JNK activation contribute to β-cell apoptosis, suggesting that ER stress in primary β-cells is primarily lipotoxic, and not glucolipotoxic. Expand
Cytokines downregulate the sarcoendoplasmic reticulum pump Ca2+ ATPase 2b and deplete endoplasmic reticulum Ca2+, leading to induction of endoplasmic reticulum stress in pancreatic beta-cells.
TLDR
The results suggest that the IL-1beta + IFN-gamma-induced decrease in SERCA2b expression, with subsequent depletion of ER Ca(2+) and activation of the ER stress pathway, is a potential contributory mechanism to beta-cell death. Expand
Impaired neuromuscular transmission and skeletal muscle fiber necrosis in mice lacking Na/Ca exchanger 3.
TLDR
It is suggested that Ca( 2+) entering nerve terminals is cleared relatively slowly in the absence of NCX3, thereby enhancing residual Ca(2+) and evoked and delayed quantal transmitter release during repetitive nerve stimulation. Expand
The pharmacokinetics of oxybutynin in man
TLDR
The low absolute systemic availability of oxybutynin, the large interindividual variability in its plasma concentrations, and the apparent absence of intact oxy butynin in the urine suggest that its major pathway of elimination is hepatic metabolism. Expand
Significance of Na/Ca exchange for Ca2+ buffering and electrical activity in mouse pancreatic beta-cells.
TLDR
Mathematical simulations suggest that the stimulatory action of glucose on beta-cell electrical activity may be accounted for in part by glucose-induced reduction of the cytoplasmic Na+ concentration with resultant activation of the exchanger. Expand
Insulin release: the fuel hypothesis.
TLDR
It is proposed that such a coupling between metabolic and cationic events is operative in response to other insulinotropic nutrients and that its time course may be relevant to the phasic aspect of insulin release. Expand
Targeted Disruption of Na+/Ca2+ Exchanger 3 (NCX3) Gene Leads to a Worsening of Ischemic Brain Damage
TLDR
It is reported that ncX3 gene suppression leads to a worsening of brain damage after focal ischemia and to a massive neuronal death in all the hippocampal fields of organotypic cultures as well as in cortical neurons from ncx3−/− mice exposed to OGD plus reoxygenation. Expand
The suppressor of cytokine signalling 2 (SOCS2) is a key repressor of insulin secretion
TLDR
SOCS2 was shown to be a potent regulator of proinsulin processing and insulin secretion in beta cells, and its constitutive production is insufficient to induce overt diabetes in this mouse model, it causes glucose intolerance. Expand
Hydroxylamine, a nitric oxide donor, inhibits insulin release and activates K+ATP channels.
TLDR
Experimental results suggest that the negative insulinotropic action of the NO donor results, at least in part, from the activation of ATP-sensitive K+ channels leading to a decrease in Ca2+ influx and [Ca2+]i. Expand
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