ArticleMolecular metabolism2015
Mice lacking neutral amino acid transporter B(0)AT1 (Slc6a19) have elevated levels of FGF21 and GLP-1 and improved glycaemic control.
Article in Molecular metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 91 citations in OpenAlex.
- Inhibitors of the Neutral Amino Acid Transporter SLC6A19 May Treat Diseases or Disorders Associated with Abnormal Amino Acid Metabolism, Epithelial Amino Acid Transport, and/or Amino Acid Levels.ACS medicinal chemistry letters · 2026Article
- Analysis of Amino Acid and Derivative Diversity and Antioxidant Capacity inJournal of fungi (Basel, Switzerland) · 2025Article
- Molecular dissection of the role of ACE2 in glucose homeostasis.Physiological reviews · 2025Review
- Combination of Berberine and Evodiamine Alleviates Obesity by Promoting Browning in 3T3-L1 Cells and High-Fat Diet-Induced Mice.International journal of molecular sciences · 2025Article
- Interaction of B0AT1 Deficiency and Diet on Metabolic Function and Diabetes Incidence in Male Nonobese Diabetic Mice.Endocrinology · 2025Article
- Western diet exacerbates a murine model of Balkan nephropathy.American journal of physiology. Renal physiology · 2025Article
- Hartnup disease-causing SLC6A19 mutations lead to B0AT1 aberrant trafficking and ACE2 mis-localisation implicating the endoplasmic reticulum protein quality control.Frontiers in cell and developmental biology · 2025Article
- Structural Dynamics of Neutral Amino Acid Transporter SLC6A19 in Simple and Complex Lipid Bilayers.Journal of cellular biochemistry · 2025Article
- Primary Roles of Branched Chain Amino Acids (BCAAs) and Their Metabolism in Physiology and Metabolic Disorders.Molecules (Basel, Switzerland) · 2024Review
- SLC6A19 inhibition facilitates urinary neutral amino acid excretion and lowers plasma phenylalanine.JCI insight · 2024Article
- State-of-the-Art-Review: Mechanisms of Action of SGLT2 Inhibitors and Clinical Implications.American journal of hypertension · 2024Review
- Molecular basis of inhibition of the amino acid transporter BNature communications · 2024Article
- Cellular mechanisms of incretin hormone secretion.Journal of molecular endocrinology · 2024Review
- Structural insight into the substrate recognition and transport mechanism of amino acid transporter complex ACE2-BCell discovery · 2023Article
- Assessment of cold exposure-induced metabolic changes in mice using untargeted metabolomics.Frontiers in molecular biosciences · 2023Article
- CRRT 2023 Meeting: Targeting Amino Acid Transport to Improve Acute Kidney Injury Outcome.Nephron · 2023Review
- Aristolochic acid-induced nephropathy is attenuated in mice lacking the neutral amino acid transporter BAmerican journal of physiology. Renal physiology · 2022Article
- Terminal Phenoxy Group as a Privileged Moiety of the Drug Scaffold-A Short Review of Most Recent Studies 2013-2022.International journal of molecular sciences · 2022Review
- Opposite physiological and pathological mTORC1-mediated roles of the CB1 receptor in regulating renal tubular function.Nature communications · 2022Article
- The central moTOR of metabolism.Developmental cell · 2022Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveType 2 diabetes arises from insulin resistance of peripheral tissues followed by dysfunction of β-cells in the pancreas due to metabolic stress. Both depletion and supplementation of neutral amino acids have been discussed as strategies to improve insulin sensitivity. Here we characterise mice lacking the intestinal and renal neutral amino acid transporter B(0)AT1 (Slc6a19) as a model to study the consequences of selective depletion of neutral amino acids.
methodsMetabolic tests, analysis of metabolite levels and signalling pathways were used to characterise mice lacking the intestinal and renal neutral amino acid transporter B(0)AT1 (Slc6a19).
resultsReduced uptake of neutral amino acids in the intestine and loss of neutral amino acids in the urine causes an overload of amino acids in the lumen of the intestine and reduced systemic amino acid availability. As a result, higher levels of glucagon-like peptide 1 (GLP-1) are produced by the intestine after a meal, while the liver releases the starvation hormone fibroblast growth factor 21 (FGF21). The combination of these hormones generates a metabolic phenotype that is characterised by efficient removal of glucose, particularly by the heart, reduced adipose tissue mass, browning of subcutaneous white adipose tissue, enhanced production of ketone bodies and reduced hepatic glucose output.
conclusionsReduced neutral amino acid availability improves glycaemic control. The epithelial neutral amino acid transporter B(0)AT1 could be a suitable target to treat type 2 diabetes.
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