ArticleThe Journal of biological chemistry2011
Obligate role for ketone body oxidation in neonatal metabolic homeostasis.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
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Who cites it
75 citing papers in PubMed, 128 citations in OpenAlex.
- Enhanced Energy Metabolism and Developmental Signaling in Neonatal Brains of Female Piglets Parenterally Fed with 18-Carbon n-3 Fatty Acid-Based Vegaven Compared with Fish Oil-Containing Lipid Emulsion.Current developments in nutrition · 2026Article
- Identification of the regulatory elements and protein substrates of lysine acetoacetylation.eLife · 2026Article
- Requirement for oxidation of neuronal ketone bodies in aging and neurodegeneration.bioRxiv : the preprint server for biology · 2026Article
- Spatiotemporal metabolic mapping reveals diet-independent remodeling of the postnatal mouse brain.npj metabolic health and disease · 2026Article
- Quantifying endogenous and tracer-derived ketone bodies using a dual-label UHPLC-MS/MS method.Talanta · 2026Article
- Human Apolipoprotein E ε4 Allele Modulates Energy Substrate Availability, Seizure Burden, Mortality and Hippocampal Injury, Cell Death, and Inflammation after Neonatal Hypoxic-Ischemic Brain Injury.Developmental neuroscience · 2026Article
- BDH1 acetylation at K116 modulates milk fat production in dairy goats.Journal of animal science and biotechnology · 2025Article
- Identification of the Regulatory Elements and Protein Substrates of Lysine Acetoacetylation.bioRxiv : the preprint server for biology · 2025Article
- Ketone Catabolism Is Essential for Maintaining Normal Heart Function During Aging.Journal of the American Heart Association · 2025Article
- The Heart Has Intrinsic Ketogenic Capacity that Mediates NADCirculation research · 2025Article
- Blood glucose and β-hydroxybutyrate predict significant brain injury after hypoxia-ischemia in neonatal mice.Pediatric research · 2025Article
- Endurance training and pyruvate dehydrogenase kinase 4 (PDK4) inhibition combination is superior to each one alone in attenuating hyperketonemia/ketoacidosis in diabetic rats.Iranian journal of basic medical sciences · 2025Article
- Ketone body oxidation and susceptibility to ethyl acetoacetate in a novel hemolytic multidrug-resistant strain Leptospira interrogans KeTo originated from sewage water.Scientific reports · 2024Article
- The Structure of the Cardiac Mitochondria Respirasome Is Adapted for the β-Oxidation of Fatty Acids.International journal of molecular sciences · 2024Review
- Ketone body metabolism and cardiometabolic implications for cognitive health.npj metabolic health and disease · 2024Article
- Identification of important modules and biomarkers in diabetic cardiomyopathy based on WGCNA and LASSO analysis.Frontiers in endocrinology · 2024Article
- Ketogenic therapy towards precision medicine for brain diseases.Frontiers in nutrition · 2024Review
- Elevated Plasma Levels of Ketone Bodies Are Associated With All-Cause Mortality and Incidence of Heart Failure in Older Adults: The CHS.Journal of the American Heart Association · 2023Article
- Glutamine metabolism in diseases associated with mitochondrial dysfunction.Molecular and cellular neurosciences · 2023Review
- [Molecular pathological mechanism of liver metabolic disorder in mice with severe spinal muscular atrophy].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023Article
15 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
To compensate for the energetic deficit elicited by reduced carbohydrate intake, mammals convert energy stored in ketone bodies to high energy phosphates. Ketone bodies provide fuel particularly to brain, heart, and skeletal muscle in states that include starvation, adherence to low carbohydrate diets, and the neonatal period. Here, we use novel Oxct1(-/-) mice, which lack the ketolytic enzyme succinyl-CoA:3-oxo-acid CoA-transferase (SCOT), to demonstrate that ketone body oxidation is required for postnatal survival in mice. Although Oxct1(-/-) mice exhibit normal prenatal development, all develop ketoacidosis, hypoglycemia, and reduced plasma lactate concentrations within the first 48 h of birth. In vivo oxidation of (13)C-labeled β-hydroxybutyrate in neonatal Oxct1(-/-) mice, measured using NMR, reveals intact oxidation to acetoacetate but no contribution of ketone bodies to the tricarboxylic acid cycle. Accumulation of acetoacetate yields a markedly reduced β-hydroxybutyrate:acetoacetate ratio of 1:3, compared with 3:1 in Oxct1(+) littermates. Frequent exogenous glucose administration to actively suckling Oxct1(-/-) mice delayed, but could not prevent, lethality. Brains of newborn SCOT-deficient mice demonstrate evidence of adaptive energy acquisition, with increased phosphorylation of AMP-activated protein kinase α, increased autophagy, and 2.4-fold increased in vivo oxidative metabolism of [(13)C]glucose. Furthermore, [(13)C]lactate oxidation is increased 1.7-fold in skeletal muscle of Oxct1(-/-) mice but not in brain. These results indicate the critical metabolic roles of ketone bodies in neonatal metabolism and suggest that distinct tissues exhibit specific metabolic responses to loss of ketone body oxidation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.