{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zweck E"],"funding":["Bundesministerium für Bildung und Forschung","Deutsche Forschungsgemeinschaft","Schmutzler Stiftung","Ministerium für Kultur und Wissenschaft des Landes Nordrhein-Westfalen","Bundesministerium für Gesundheit","German Heart Foundation","Deutsches Zentrum für Diabetesforschung","European Commission","German Diabetes Society"],"pagination":["106007"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12657344"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["122"],"pubmed_abstract":["<h4>Background</h4>Reduced mitochondrial respiratory function has been implicated in metabolic disorders like type 2 diabetes (T2D), obesity, and metabolic dysfunction-associated steatotic liver disease (MASLD), which are tightly linked to insulin resistance and impaired metabolic flexibility. However, the contribution of the ketone bodies (KBs) β-hydroxybutyrate (HBA) and acetoacetate (ACA) as substrates for mitochondrial oxidative phosphorylation (OXPHOS) in these insulin resistant states remains unclear.<h4>Methods</h4>Targeted high-resolution respirometry protocols were applied to detect the differential contribution of HBA and ACA to OXPHOS capacity in heart, skeletal muscle, kidney, and liver of distinct human or murine cohorts with T2D, obesity, and MASLD.<h4>Findings</h4>In humans "],"journal":["EBioMedicine"],"pubmed_title":["Impaired mitochondrial ketone body oxidation in insulin resistant states."],"pmcid":["PMC12657344"],"funding_grant_id":["493659010","527448911","HORIZON-HLTH-2022-STAYHLTH-02-01","2020","236177352","F/22/18","CRC1116"],"pubmed_authors":["Scheiber D","Dewidar B","Al-Hasani H","Schmidt JW","Roden M","Remus R","Schon M","Granata C","Mastrototaro L","Piel S","Aubin H","Zweck E","Kahl S","Westenfeld R","Chadt A","Wagner R","Distler J","Kelm M","Polzin A","Szendroedi J","Burkart V","Lichtenberg A","Schrauwen P","Boeken U"],"additional_accession":[]},"is_claimable":false,"name":"Impaired mitochondrial ketone body oxidation in insulin resistant states.","description":"<h4>Background</h4>Reduced mitochondrial respiratory function has been implicated in metabolic disorders like type 2 diabetes (T2D), obesity, and metabolic dysfunction-associated steatotic liver disease (MASLD), which are tightly linked to insulin resistance and impaired metabolic flexibility. However, the contribution of the ketone bodies (KBs) β-hydroxybutyrate (HBA) and acetoacetate (ACA) as substrates for mitochondrial oxidative phosphorylation (OXPHOS) in these insulin resistant states remains unclear.<h4>Methods</h4>Targeted high-resolution respirometry protocols were applied to detect the differential contribution of HBA and ACA to OXPHOS capacity in heart, skeletal muscle, kidney, and liver of distinct human or murine cohorts with T2D, obesity, and MASLD.<h4>Findings</h4>In humans ","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Nov","modification":"2026-06-06T07:05:53.318Z","creation":"2026-06-06T03:06:24.344Z"},"accession":"S-EPMC12657344","cross_references":{"pubmed":["41223787"],"doi":["10.1016/j.ebiom.2025.106007"]}}