ArticleCPT: pharmacometrics & systems pharmacology2016
Model-Based Assessment of Plasma Citrate Flux Into the Liver: Implications for NaCT as a Therapeutic Target.
Article in CPT: pharmacometrics & systems pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 27 citations in OpenAlex.
- Hydrogen Sulfide (HAntioxidants (Basel, Switzerland) · 2025Article
- Targeting Longevity GeneMetabolites · 2023Article
- Double-edged effect of sodium citrate in Nile tilapia (Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2023Article
- Rumen microbial-driven metabolite from grazing lambs potentially regulates body fatty acid metabolism by lipid-related genes in liver.Journal of animal science and biotechnology · 2023Article
- Extracellular citrate and metabolic adaptations of cancer cells.Cancer metastasis reviews · 2021Review
- Serum Metabolomic Profiling to Reveal Potential Biomarkers for the Diagnosis of Fatty Liver Hemorrhagic Syndrome in Laying Hens.Frontiers in physiology · 2021Article
- Plasma Krebs Cycle Intermediates in Nonalcoholic Fatty Liver Disease.Journal of clinical medicine · 2020Article
- Metabolomics Characterizes the Effects and Mechanisms of Quercetin in Nonalcoholic Fatty Liver Disease Development.International journal of molecular sciences · 2019Article
- SuppressedFEBS open bio · 2018Article
- Characteristics of hepatic insulin-sensitive nonalcoholic fatty liver disease.Hepatology communications · 2017Article
- Plasma Membrane Na⁺-Coupled Citrate Transporter (SLC13A5) and Neonatal Epileptic Encephalopathy.Molecules (Basel, Switzerland) · 2017Review
- Mutations in the Na(+)/citrate cotransporter NaCT (SLC13A5) in pediatric patients with epilepsy and developmental delay.Molecular medicine (Cambridge, Mass.) · 2016Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cytoplasmic citrate serves as an important regulator of gluconeogenesis and carbon source for de novo lipogenesis in the liver. For this reason, the sodium-coupled citrate transporter (NaCT), a plasma membrane transporter that governs hepatic influx of plasma citrate in human, is being explored as a potential therapeutic target for metabolic disorders. As cytoplasmic citrate also originates from intracellular mitochondria, the relative contribution of these two pathways represents critical information necessary to underwrite confidence in this target. In this work, hepatic influx of plasma citrate was quantified via pharmacokinetic modeling of published clinical data. The influx was then compared to independent literature estimates of intracellular citrate flux in human liver. The results indicate that, under normal conditions, <10% of hepatic citrate originates from plasma. Similar estimates were determined experimentally in mice and rats. This suggests that NaCT inhibition will have a limited impact on hepatic citrate concentrations across species.
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Registered trials
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