ArticleThe Biochemical journal2006
The case for regulating indispensable amino acid metabolism: the branched-chain alpha-keto acid dehydrogenase kinase-knockout mouse.
Article in The Biochemical journal, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 25 citations in OpenAlex.
- Apparent Saturation of Branched-Chain Amino Acid Catabolism After High Dietary Milk Protein Intake in Healthy Adults.The Journal of clinical endocrinology and metabolism · 2025Trial
- Classical maple syrup urine disease and brain development: principles of management and formula design.Molecular genetics and metabolism · 2010Trial
- BCKDK gene mutations as a rare condition responsible for comorbid neurodevelopmental delay, autism, and epilepsy: a case series of four patients.Annals of medicine and surgery (2012) · 2025Article
- Article
- Influence of the Gut Microbiome on Feed Intake of Farm Animals.Microorganisms · 2022Review
- BCAT1 promotes osteoclast maturation by regulating branched-chain amino acid metabolism.Experimental & molecular medicine · 2022Article
- Multiomics-Identified Intervention to Restore Ethanol-Induced Dysregulated Proteostasis and Secondary Sarcopenia in Alcoholic Liver Disease.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2021Article
- Oxoeicosanoid receptor inhibition alleviates acute myocardial infarction through activation of BCAT1.Basic research in cardiology · 2021Article
- Article
- L-leucine stimulates glutamate dehydrogenase activity and glutamate synthesis by regulating mTORC1/SIRT4 pathway in pig liver.Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2018Article
- BCAT1 controls metabolic reprogramming in activated human macrophages and is associated with inflammatory diseases.Nature communications · 2017Article
- Branched-Chain Amino Acids and Brain Metabolism.Neurochemical research · 2017Review
- A single transcription factor is sufficient to induce and maintain secretory cell architecture.Genes & development · 2017Article
- Article
- Mechanisms of the pellagragenic effect of leucine: stimulation of hepatic tryptophan oxidation by administration of branched-chain amino acids to healthy human volunteers and the role of plasma free tryptophan and total kynurenines.International journal of tryptophan research : IJTR · 2014Article
- Novel nutritional treatment for manic and psychotic disorders: a review of tryptophan and tyrosine depletion studies and the potential of protein-based formulations using glycomacropeptide.Psychopharmacology · 2013Review
- BCAT1 promotes cell proliferation through amino acid catabolism in gliomas carrying wild-type IDH1.Nature medicine · 2013Article
- Pathogenesis of A⁻β⁺ ketosis-prone diabetes.Diabetes · 2013Article
- Triennial Growth Symposium: leucine acts as a nutrient signal to stimulate protein synthesis in neonatal pigs.Journal of animal science · 2011Review
- Specificity of the Acute Tryptophan and Tyrosine Plus Phenylalanine Depletion and Loading Tests Part II: Normalisation of the Tryptophan and the Tyrosine Plus Phenylalanine to Competing Amino Acid Ratios in a New Control Formulation.International journal of tryptophan research : IJTR · 2010Article
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1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BCAAs (branched-chain amino acids) are indispensable (essential) amino acids that are required for body protein synthesis. Indispensable amino acids cannot be synthesized by the body and must be acquired from the diet. The BCAA leucine provides hormone-like signals to tissues such as skeletal muscle, indicating overall nutrient sufficiency. BCAA metabolism provides an important transport system to move nitrogen throughout the body for the synthesis of dispensable (non-essential) amino acids, including the neurotransmitter glutamate in the central nervous system. BCAA metabolism is tightly regulated to maintain levels high enough to support these important functions, but at the same time excesses are prevented via stimulation of irreversible disposal pathways. It is well known from inborn errors of BCAA metabolism that dysregulation of the BCAA catabolic pathways that leads to excess BCAAs and their alpha-keto acid metabolites results in neural dysfunction. In this issue of Biochemical Journal, Joshi and colleagues have disrupted the murine BDK (branched-chain alpha-keto acid dehydrogenase kinase) gene. This enzyme serves as the brake on BCAA catabolism. The impaired growth and neurological abnormalities observed in this animal show conclusively the importance of tight regulation of indispensable amino acid metabolism.
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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.