ArticleNature communications2024
SLC17A1/3 transporters mediate renal excretion of Lac-Phe in mice and humans.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Exerkines in precision management of metabolic diseases.Chinese medical journal · 2026Review
- The SLC-ome of membrane transport: from molecular discovery to physiology and clinical applications.Physiological reviews · 2026Review
- Lactate as a Chemical Modification on Proteins and Metabolites.Annual review of biochemistry · 2026Review
- The Emerging Role of N-Lactoyl-Phenylalanine (Lac-Phe) in Metabolic Regulation and Disease: From Exercise-Induced Metabolite to Therapeutic Candidate.Antioxidants (Basel, Switzerland) · 2026Article
- Beyond exercise and appetite: The expanding biology and therapeutic potential of N-lactoyl-phenylalanine.The Journal of pharmacology and experimental therapeutics · 2026Review
- Lac-Phe: An Emerging Appetite-Regulating Exerkine with Health and Therapeutic Benefits.Current obesity reports · 2026Review
- Untargeted Metabolomic Study for Urinary Characterization of Adult Patients with Phenylketonuria.International journal of molecular sciences · 2025Article
- Article
- N-Lactoyl Amino Acids: Emerging Biomarkers in Metabolism and Disease.Diabetes/metabolism research and reviews · 2025Review
- Review
- Integrative causal inference and predictive modeling reveal the iron-related gene SLC17A4 as a key biomarker in chronic rhinosinusitis.Frontiers in immunology · 2025Article
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10 authors.
Funding
Abstract
N-lactoyl-phenylalanine (Lac-Phe) is a lactate-derived metabolite that suppresses food intake and body weight. Little is known about the mechanisms that mediate Lac-Phe transport across cell membranes. Here we identify SLC17A1 and SLC17A3, two kidney-restricted plasma membrane-localized solute carriers, as physiologic urine Lac-Phe transporters. In cell culture, SLC17A1/3 exhibit high Lac-Phe efflux activity. In humans, levels of Lac-Phe in urine exhibit a strong genetic association with the SLC17A1-4 locus. Urine Lac-Phe levels are increased following a Wingate sprint test. In mice, genetic ablation of either SLC17A1 or SLC17A3 reduces urine Lac-Phe levels. Despite these differences, both knockout strains have normal blood Lac-Phe and body weights, demonstrating SLC17A1/3-dependent de-coupling of urine and plasma Lac-Phe pools. Together, these data establish SLC17A1/3 family members as the physiologic urine Lac-Phe transporters and uncover a biochemical pathway for the renal excretion of this signaling metabolite.
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