The coupling of metabolic to secretory events in pancreatic islets. The possible role of glutathione reductase.

@article{Malaisse1985TheCO,
  title={The coupling of metabolic to secretory events in pancreatic islets. The possible role of glutathione reductase.},
  author={Willy J Malaisse and Simon Dufrane and Paulo Cezar de Freitas Mathias and Angelo Rafael Carpinelli and Francine Malaisse-Lagae and Pilar Garc{\'i}a-Morales and Isabel Valverde and Abdullah Sener},
  journal={Biochimica et biophysica acta},
  year={1985},
  volume={844 2},
  pages={
          256-64
        }
}
Glutathione reductase is expressed at high levels in pancreatic islet cells
TLDR
The levels of antioxidant/redox proteins, peroxiredoxins-1, -4, and -6 and glutathione reductase (GR) were examined by immunohistochemistry and found that the expression of GR was very high in pancreatic islet cells compared to exocrine cells, pointing to a pivotal role of the glutATHione redox system in pancreatIC islet Cells against diabetogenic stress.
Insights into the critical role of NADPH oxidase(s) in the normal and dysregulated pancreatic beta cell
TLDR
Recent information and evidence of NADPH oxidase-dependent generation of ROS in pancreatic beta cells are described and the various beta cell isoforms may, via differences in the kinetics and species of ROS generated, positively and negatively regulate insulin secretion and cell survival are identified.
Effect of Sulfhydryl Reagents on Pancreatic Islet Secretion Granule–Plasma Membrane Interaction
TLDR
It is concluded that the presence of a preponderance of sulfhydryl groups on the secretion granule membranes tends to limit their interaction with the plasma membrane and that these must be removed or masked for maximum fusion to occur.
Effects of pharmacological inhibition of NADPH oxidase or iNOS on pro-inflammatory cytokine, palmitic acid or H2O2-induced mouse islet or clonal pancreatic β-cell dysfunction.
TLDR
It is reported that H( 2)O(2) can increase levels of the latter two proteins, suggesting a key role for positive-feedback redox sensitive regulation of β-cell dysfunction.
13C NMR analysis reveals a link between L-glutamine metabolism, D-glucose metabolism and γ-glutamyl cycle activity in a clonal pancreatic beta-cell line
TLDR
It is proposed that L-glutamine metabolism is important in the beta cell for generation of stimulus-secretion coupling factors, precursors of glutathione synthesis and for supplying carbon for oxidation in the TCA cycle.
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It is suggested that a transfer of reducing equivalents to extramitochondrial sites participates in the process of insulin release, whether the latter involves the oxidation of exogenous or endogenous nutrients.
The stimulus-secretion coupling of glucose-induced insulin release. Metabolic effects of menadione in isolated islets.
TLDR
When insulinotropic nutrients are oxidized in the B-cell, the increased availability of reduced pyridine nucleotides could modify the affinity for cations of native ionophoretic systems, eventually leading to the accumulation of calcium up to a level sufficient to trigger insulin release.
The stimulus-secretion coupling of glucose-induced insulin release. Metabolic events in islets stimulated by non-metabolizable secretagogues.
TLDR
The data indicate that insulin release can be stimulated by non‐metabolizable secretagogues, despite a fall in the concentration of both ATP and NAD(P)H, however, the insulinotropic action of glucose, whatever its concentration, may depend on an increased generation of both reducing equivalents and high‐energy phosphate intermediates.
The coupling of metabolic to secretory events in pancreatic islets. The cytosolic redox state.
TLDR
The cytosolic generation of NADPH, e.g. at the level of the malic enzyme, may play a role in the coupling of metabolic to secretory events in the process of nutrient-stimulated insulin release.
The stimulus-secretion coupling of glucose-induced insulin release. Cationic and secretory effects of menadione in the endocrine pancreas.
TLDR
It is concluded that menadione impairs the insulinotropic action of glucose and other nutrients by impeding the remodelling of cationic fluxes normally provoked by these secretagogues in islet cells.
The stimulus-secretion coupling of glucose-induced insulin release. LIII. Calcium-dependency of the cyclic AMP response to nutrient secretagogues.
TLDR
Findings are compatible with the view that an increase in the generation rate of cyclic AMP participates in the process of nutrient-stimulated insulin release and could be secondary to the nutrient-induced accumulation of Ca2+ in the islet cells leading to activation of adenylate cyclase by calmodulin.
The Stimulus-Secretion Coupling of Amino Acid-induced Insulin Release: Secretory and Oxidative Response of Pancreatic Islets to L-Asparagine
TLDR
It is proposed that the enhancing action of L-asparagine upon insulin release evoked by L-leucine might be due to an accelerated generation rate of cytosolic NAOPH, rather than to any sizable increase in either islet respiration or steady-state cytosol NADPH/NADP+ ratio.
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