ArticlePflugers Archiv : European journal of physiology2016
Loss of function mutation of the Slc38a3 glutamine transporter reveals its critical role for amino acid metabolism in the liver, brain, and kidney.
Article in Pflugers Archiv : European journal of physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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36 citing papers in PubMed, 51 citations in OpenAlex.
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- The Glutamate/GABA-Glutamine Cycle: Insights, Updates, and Advances.Journal of neurochemistry · 2025Review
- Traditional Chinese Medicine in the Comprehensive Management of Tourette Syndrome: Insights from Genetics and Pathophysiology: A Review.Drug design, development and therapy · 2025Review
- A machine learning-based immune response signature to facilitate prognosis prediction in patients with endometrial cancer.Scientific reports · 2024Article
- A genome-wide association study of the racing performance traits in Yili horses based on Blink and FarmCPU models.Scientific reports · 2024Article
- State of knowledge on ammonia handling by the kidney.Pflugers Archiv : European journal of physiology · 2024Review
- Glutamine transporter SLC38A3 promotes breast cancer metastasis via Gsk3β/β-catenin/EMT pathway.Cancer letters · 2024Article
- The effect of genetic variants of SLC22A18 on proliferation, migration, and invasion of colon cancer cells.Scientific reports · 2024Article
- Proteomic alterations in the brain and blood-brain barrier during brain Aβ accumulation in an APP knock-in mouse model of Alzheimer's disease.Fluids and barriers of the CNS · 2023Article
- Biallelic variants in SLC38A3 encoding a glutamine transporter cause epileptic encephalopathy.Brain : a journal of neurology · 2022Article
- Unconventional Functions of Amino Acid Transporters: Role in Macropinocytosis (SLC38A5/SLC38A3) and Diet-Induced Obesity/Metabolic Syndrome (SLC6A19/SLC6A14/SLC6A6).Biomolecules · 2022Review
- SLC38A10 Knockout Mice Display a Decreased Body Weight and an Increased Risk-Taking Behavior in the Open Field Test.Frontiers in behavioral neuroscience · 2022Article
- Contributions of SGK3 to transporter-related diseases.Frontiers in cell and developmental biology · 2022Review
- Solute carrier transporter disease and developmental and epileptic encephalopathy.Frontiers in neurology · 2022Review
- Enhanced supply of methionine regulates protein synthesis in bovine mammary epithelial cells under hyperthermia condition.Journal of animal science and technology · 2021Article
- The role of the glutamine transporter ASCT2 in antineoplastic therapy.Cancer chemotherapy and pharmacology · 2021Review
- Comprehensive Analysis of the Expression Profiles of Hepatic lncRNAs in the Mouse Model of Alcoholic Liver Disease.Frontiers in pharmacology · 2021Article
- Structural and biochemical imaging reveals systemic LPS-induced changes in the rat brain.Journal of neuroimmunology · 2020Article
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glutamine, the most abundant amino acid in mammals, is critical for cell and organ functions. Its metabolism depends on the ability of cells to take up or release glutamine by transporters located in the plasma membrane. Several solute carrier (SLC) families transport glutamine, but the SLC38 family has been thought to be mostly responsible for glutamine transport. We demonstrate that despite the large number of glutamine transporters, the loss of Snat3/Slc38a3 glutamine transporter has a major impact on the function of organs expressing it. Snat3 mutant mice were generated by N-ethyl-N-nitrosurea (ENU) mutagenesis and showed stunted growth, altered amino acid levels, hypoglycemia, and died around 20 days after birth. Hepatic concentrations of glutamine, glutamate, leucine, phenylalanine, and tryptophan were highly reduced paralleled by downregulation of the mTOR pathway possibly linking reduced amino acid availability to impaired growth and glucose homeostasis. Snat3-deficient mice had altered urea levels paralleled by dysregulation of the urea cycle, gluconeogenesis, and glutamine synthesis. Mice were ataxic with higher glutamine but reduced glutamate and gamma-aminobutyric acid (GABA) levels in brain consistent with a major role of Snat3 in the glutamine-glutamate cycle. Renal ammonium excretion was lower, and the expression of enzymes and amino acid transporters involved in ammoniagenesis were altered. Thus, SNAT3 is a glutamine transporter required for amino acid homeostasis and determines critical functions in various organs. Despite the large number of glutamine transporters, loss of Snat3 cannot be compensated, suggesting that this transporter is a major route of glutamine transport in the liver, brain, and kidney.
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