ArticleProceedings of the National Academy of Sciences of the United States of America2002
Neonatal hepatic steatosis by disruption of the adenosine kinase gene.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 papers.
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121 citing papers in PubMed, 221 citations in OpenAlex.
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- Adenosine metabolic clearance maintains liver homeostasis by licensing arginine methylation of RIPK1.The Journal of experimental medicine · 2026Article
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- High Fat Low Carbohydrate Diet Is Linked to CNS Autoimmunity Protection.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Sudden Unexpected Death in Epilepsy: A Narrative Review of Mechanism, Risks, and Prevention.Journal of clinical medicine · 2025Review
- Adenosine Kinase: An Epigenetic Modulator and Drug Target.Journal of inherited metabolic disease · 2025Review
- NRH, a potent NADMetabolism: clinical and experimental · 2025Article
- Neuroglia and brain energy metabolism.Handbook of clinical neurology · 2025Review
- Disruption of adenosine metabolism increases risk of seizure-induced death despite decreased seizure severity.Epilepsia · 2024Article
- Investigating open access new approach methods (NAM) to assess biological points of departure: A case study with 4 neurotoxic pesticides.Current research in toxicology · 2024Article
- Developmental and foliation changes due to dysregulation of adenosine kinase in the cerebellum.Scientific reports · 2023Article
- Electrospun PVA Fibers for Drug Delivery: A Review.Polymers · 2023Review
- Inborn Errors of Purine Salvage and Catabolism.Metabolites · 2023Review
- Molecular and Pathological Analyses of IARS1-Deficient Mice: An IARS Disorder Model.International journal of molecular sciences · 2023Article
- Astrocyte-neuron circuits in epilepsy.Neurobiology of disease · 2023Review
- Review
61 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
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Abstract
Neonatal hepatic steatosis (OMIM 228100) is a fatal condition of unknown etiology characterized by a pale and yellow liver and early postnatal mortality. In the present study, a deficit in adenosine-dependent metabolism is proposed as a causative factor. Physiologically, adenosine is efficiently metabolized to AMP by adenosine kinase (ADK), an enzyme highly expressed in liver. ADK not only ensures normal adenine nucleotide levels but also is essential for maintaining S-adenosylmethionine-dependent transmethylation processes, where adenosine, an obligatory product, has to be constantly removed. Homozygous Adk(-/-) mutants developed normally during embryogenesis. However, within 4 days after birth they displayed microvesicular hepatic steatosis and died within 14 days with fatty liver. Adenine nucleotides were decreased and S-adenosylhomocysteine, a potent inhibitor of transmethylation reactions, was increased in the mutant liver. Thus, a deficiency in adenosine metabolism is identified as a powerful contributor to the development of neonatal hepatic steatosis, providing a model for the rapid development of postnatally lethal fatty liver.
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