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TITLE:
Combined metabolic activators decrease liver steatosis by activating mitochondrial metabolism in hamsters fed with a high-fat diet - imarina:9230636

URV's Author/s:Arola Ferrer, Luis Maria / Del Bas Prior, José María
Author, as appears in the article.:Yang, Hong; Mayneris-Perxachs, Jordi; Boque, Noemi; del Bas, Josep M; Arola, Lluis; Yuan, Meng; Tuerkez, Hasan; Uhlen, Mathias; Boren, Jan; Zhang, Cheng; Mardinoglu, Adil; Caimari, Antoni
Author's mail:josepm.delbas@urv.cat
lluis.arola@urv.cat
Author identifier:0000-0003-2767-1974
Journal publication year:2021
Publication Type:Journal Publications
APA:Yang, Hong; Mayneris-Perxachs, Jordi; Boque, Noemi; del Bas, Josep M; Arola, Lluis; Yuan, Meng; Tuerkez, Hasan; Uhlen, Mathias; Boren, Jan; Zhang, Che (2021). Combined metabolic activators decrease liver steatosis by activating mitochondrial metabolism in hamsters fed with a high-fat diet. Biomedicines, 9(10), 1440-. DOI: 10.3390/biomedicines9101440
Paper original source:Biomedicines. 9 (10): 1440-
Abstract:Although the prevalence of non-alcoholic fatty liver disease (NAFLD) continues to increase, there is no effective treatment approved for this condition. We previously showed, in high-fat diet (HFD)-fed mice, that the supplementation of combined metabolic activators (CMA), including nicotinamide riboside (NAD+ precursor) and the potent glutathione precursors serine and N-acetyl-l-cysteine (NAC), significantly decreased fatty liver by promoting fat oxidation in mitochondria. Afterwards, in a one-day proof-of-concept human supplementation study, we observed that this CMA, including also L-carnitine tartrate (LCT), resulted in increased fatty acid oxidation and de novo glutathione synthesis. However, the underlying molecular mechanisms associated with sup-plementation of CMA have not been fully elucidated. Here, we demonstrated in hamsters that the chronic supplementation of this CMA (changing serine for betaine) at two doses significantly decreased hepatic steatosis. We further generated liver transcriptomics data and integrated these data using a liver-specific genome-scale metabolic model of liver tissue. We systemically determined the molecular changes after the supplementation of CMA and found that it activates mitochondria in the liver tissue by modulating global lipid, amino acid, antioxidant and folate metabolism. Our findings provide extra evidence about the beneficial effects of a treatment based on this CMA against NAFLD.
Article's DOI:10.3390/biomedicines9101440
Link to the original source:https://www.mdpi.com/2227-9059/9/10/1440
Paper version:info:eu-repo/semantics/publishedVersion
licence for use:https://creativecommons.org/licenses/by/3.0/es/
Department:Bioquímica i Biotecnologia
Licence document URL:https://repositori.urv.cat/ca/proteccio-de-dades/
Thematic Areas:Pharmacology & pharmacy
Medicine, research & experimental
Medicine (miscellaneous)
General biochemistry,genetics and molecular biology
Ciencias sociales
Biochemistry, genetics and molecular biology (miscellaneous)
Biochemistry, genetics and molecular biology (all)
Biochemistry & molecular biology
Keywords:Transcriptomics
Oxidative stress
Nafld
Mitochondrial metabolism
Combined metabolic activators
vitamin-c
transcriptomics
protects
peroxisome
obesity
mitochondrial metabolism
insulin-resistance
expression
disease
deficiency
combined metabolic activators
acid oxidation
Entity:Universitat Rovira i Virgili
Record's date:2025-02-18
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