Title : Interplay between NADH oxidation by complex I, glutathione redox state and sirtuin-3, and its role in the development of insulin resistance.

Pub. Date : 2020 Aug 1

PMID : 32305451






5 Functional Relationships(s)
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Protein Name
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1 Metabolic diseases are characterized by high NADH/NAD+ ratios due to excessive electron supply, causing defective mitochondrial function and impaired sirtuin-3 (SIRT-3) activity, the latter driving to oxidative stress and altered fatty acid beta-oxidation. NAD sirtuin 3 Homo sapiens
2 Metabolic diseases are characterized by high NADH/NAD+ ratios due to excessive electron supply, causing defective mitochondrial function and impaired sirtuin-3 (SIRT-3) activity, the latter driving to oxidative stress and altered fatty acid beta-oxidation. NAD sirtuin 3 Homo sapiens
3 NADH is oxidized by the complex I in the electron transport chain, thereby factors inhibiting complex I like acetylation, cardiolipin peroxidation, and glutathionylation by low GSH/GSSG ratios affects SIRT3 function by increasing the NADH/NAD+ ratio. NAD sirtuin 3 Homo sapiens
4 NADH is oxidized by the complex I in the electron transport chain, thereby factors inhibiting complex I like acetylation, cardiolipin peroxidation, and glutathionylation by low GSH/GSSG ratios affects SIRT3 function by increasing the NADH/NAD+ ratio. NAD sirtuin 3 Homo sapiens
5 NADH is oxidized by the complex I in the electron transport chain, thereby factors inhibiting complex I like acetylation, cardiolipin peroxidation, and glutathionylation by low GSH/GSSG ratios affects SIRT3 function by increasing the NADH/NAD+ ratio. NAD sirtuin 3 Homo sapiens