{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Arc-Chagnaud C"],"funding":["Instituto de Salud Carlos III","Ministerio de Ciencia e Innovación","Montana Department of Agriculture","Advanced Foods and Materials Canada","Fundació la Marató de TV3","Fundación General CSIC","Generalitat Valenciana","European Regional Development Fund"],"pagination":["1879-1896"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8718080"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["12(6)"],"pubmed_abstract":["<h4>Background</h4>Frailty is a major age-associated syndrome leading to disability. Oxidative damage plays a significant role in the promotion of frailty. The cellular antioxidant system relies on reduced nicotinamide adenine dinucleotide phosphate (NADPH) that is highly dependent on glucose 6-P dehydrogenase (G6PD). The G6PD-overexpressing mouse (G6PD-Tg) is protected against metabolic stresses. Our aim was to examine whether this protection delays frailty.<h4>Methods</h4>Old wild-type (WT) and G6PD-Tg mice were evaluated longitudinally in terms of frailty. Indirect calorimetry, transcriptomic profile, and different skeletal muscle quality markers and muscle regenerative capacity were also investigated.<h4>Results</h4>The percentage of frail mice was significantly lower in the G6PD-Tg th"],"journal":["Journal of cachexia, sarcopenia and muscle"],"pubmed_title":["Glucose 6-P dehydrogenase delays the onset of frailty by protecting against muscle damage."],"pmcid":["PMC8718080"],"funding_grant_id":["202033","CB16/10/00435"],"pubmed_authors":["Arc-Chagnaud C","Serna E","Gomez-Cabrera MC","Garcia-Dominguez E","Vina J","Correas AG","Chopard A","Munoz-Canoves P","Sebastia V","Salvador-Pascual A","Fernandez-Marcos PJ","Olaso-Gonzalez G","Brioche T","Serrano AL","Serrano M"],"additional_accession":[]},"is_claimable":false,"name":"Glucose 6-P dehydrogenase delays the onset of frailty by protecting against muscle damage.","description":"<h4>Background</h4>Frailty is a major age-associated syndrome leading to disability. Oxidative damage plays a significant role in the promotion of frailty. The cellular antioxidant system relies on reduced nicotinamide adenine dinucleotide phosphate (NADPH) that is highly dependent on glucose 6-P dehydrogenase (G6PD). The G6PD-overexpressing mouse (G6PD-Tg) is protected against metabolic stresses. Our aim was to examine whether this protection delays frailty.<h4>Methods</h4>Old wild-type (WT) and G6PD-Tg mice were evaluated longitudinally in terms of frailty. Indirect calorimetry, transcriptomic profile, and different skeletal muscle quality markers and muscle regenerative capacity were also investigated.<h4>Results</h4>The percentage of frail mice was significantly lower in the G6PD-Tg th","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Dec","modification":"2026-05-09T11:56:46.743Z","creation":"2022-02-11T15:04:08.992Z"},"accession":"S-EPMC8718080","cross_references":{"pubmed":["34704386"],"doi":["10.1002/jcsm.12792"]}}