Literature summary for 7.1.1.1 extracted from

Navarro, C.D.C.; Figueira, T.R.; Francisco, A.; DalBo, G.A.; Ronchi, J.A.; Rovani, J.C.; Escanhoela, C.A.F.; Oliveira, H.C.F.; Castilho, R.F.; Vercesi, A.E.
Redox imbalance due to the loss of mitochondrial NAD(P)-transhydrogenase markedly aggravates high fat diet-induced fatty liver disease in mice (2017), Free Radic. Biol. Med., 113, 190-202 .

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Application

Application	Comment	Organism
medicine	after 20 weeks on a high-fat diet, Nnt-/- mice exhibit a higher prevalence of steatohepatitis and content of liver triglycerides compared to Nnt+/+ mice on an identical diet. Under a a high-fat diet, the aggravated non-alcoholic fatty liver disease phenotype in the Nnt-/- mice is accompanied by an increased H2O2 release rate from mitochondria, decreased aconitase activity and higher susceptibility to Ca2+-induced mitochondrial permeability transition. A high-fat diet leads to the phosphorylation (inhibition) of pyruvate dehydrogenase and markedly reduces the ability of liver mitochondria to remove peroxide in Nnt-/- mice. Compared to mice that are chow-fed, a high-fat diet does not impair peroxide removal nor elicit redox imbalance in mitochondria from Nnt+/+ mice	Mus musculus

Localization

Localization	Comment	Organism	GeneOntology No.	Textmining
mitochondrion	-	Mus musculus	5739	-

Organism

Organism	UniProt	Comment	Textmining
Mus musculus	Q61941	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
liver	-	Mus musculus	-

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Release 2023.1 (January 2023)