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Literature summary for 7.1.1.1 extracted from

  • Santos, L.R.B.; Muller, C.; de Souza, A.H.; Takahashi, H.K.; Spegel, P.; Sweet, I.R.; Chae, H.; Mulder, H.; Jonas, J.C.
    NNT reverse mode of operation mediates glucose control of mitochondrial NADPH and glutathione redox state in mouse pancreatic beta-cells (2017), Mol. Metab., 6, 535-547 .
    View publication on PubMedView publication on EuropePMC
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Organism

Organism UniProt Comment Textmining
Mus musculus Q61941
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Source Tissue

Source Tissue Comment Organism Textmining
pancreatic islet
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 Mus musculus
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Synonyms

Synonyms Comment Organism
nicotinamide nucleotide transhydrogenase
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 Mus musculus
NNT
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 Mus musculus

General Information

General Information Comment Organism
physiological function NNT is largely responsible for the acute glucose-induced rise in pancreatic islet NADPH/NADP+ ratio and decrease in mitochondrial glutathione oxidation, with a small impact on cytosolic glutathione. These effects results from a glucose-dependent reduction in NADPH consumption by NNT reverse mode of operation, rather than from a stimulation of its forward mode of operation. Lack of NNT in islets decreases their sensitivity to exogenous H2O2 at non-stimulating glucose. The lack of NNT does not alter the glucose-stimulation of Ca2+ influx and upstream mitochondrial events, but it markedly reduces both phases of glucose stimulation of insulin secretion by altering Ca2+-induced exocytosis and its metabolic amplification Mus musculus