Component

Human sodium-coupled citrate transporter / SLC13A5

Context-specific entity; species, compartment and exposure are stated on each claim.

4 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What it acts on

  1. Lithium increased NaCT-mediated use of extracellular citrate for lipid synthesis in human liver cells.

    Human sodium-coupled citrate transporter / SLC13A5 → Human liver-cell extracellular-citrate incorporation into lipids source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human liver-cell tracer/transport study.
    limitations
    Does not establish that this pathway explains clinical weight change.
    nutrient_topic
    Lithium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Lithium
    plain_language
    Transported citrate can enter lipid-building pathways.
    primary_references
    Human sodium-coupled citrate transporter, the orthologue of Drosophila Indy, as a novel target for lithium action. · 2003 · https://pubmed.ncbi.nlm.nih.gov/12826022/ · DOI 10.1042/BJ20030827

    Lithium: metal-sensitive enzymes, transport and cross-nutrient mechanisms (2026-09-19) · lines 272–278

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human liver-cell tracer/transport study. · source_derived_draft · unverified_draft

    ## lithium-nact-lipids Transported citrate can enter lipid-building pathways. Lithium increased NaCT-mediated use of extracellular citrate for lipid synthesis in human liver cells. Model: Human liver-cell tracer/transport study. Limitations: Does not establish that this pathway explains clinical weight change. Evidence access: Primary abstract Human sodium-coupled citrate transporter, the orthologue of Drosophila Indy, as a novel target for lithium action. · 2003 · https://pubmed.ncbi.nlm.nih.gov/12826022/ · DOI 10.1042/BJ20030827
    Complete structured claim and evidence

What acts on it

  1. Lithium shifted human NaCT toward higher substrate affinity and lower transport capacity.

    Lithium ion (Li+) → Human sodium-coupled citrate transporter / SLC13A5 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Cloned human transporter kinetic analysis.
    limitations
    Net flux depends on citrate and ion concentrations; not unconditional stimulation at every substrate level.
    nutrient_topic
    Lithium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Lithium
    plain_language
    A stronger apparent response can coexist with a lower maximum rate.
    primary_references
    Species-specific influence of lithium on the activity of SLC13A5 (NaCT): lithium-induced activation is specific for the transporter in primates. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25617245/ · DOI 10.1124/jpet.114.221523

    Lithium: metal-sensitive enzymes, transport and cross-nutrient mechanisms (2026-09-19) · lines 288–294

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Cloned human transporter kinetic analysis. · source_derived_draft · unverified_draft

    ## lithium-nact-affinity A stronger apparent response can coexist with a lower maximum rate. Lithium shifted human NaCT toward higher substrate affinity and lower transport capacity. Model: Cloned human transporter kinetic analysis. Limitations: Net flux depends on citrate and ion concentrations; not unconditional stimulation at every substrate level. Evidence access: Primary abstract Species-specific influence of lithium on the activity of SLC13A5 (NaCT): lithium-induced activation is specific for the transporter in primates. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25617245/ · DOI 10.1124/jpet.114.221523
    Complete structured claim and evidence

  2. Lithium stimulated human NaCT-mediated citrate transport at concentrations relevant to prescription exposure.

    Lithium ion (Li+) → Human sodium-coupled citrate transporter / SLC13A5 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Expressed human transporter and human liver-cell experiments.
    limitations
    Not evidence that trace lithium has the same effect or that citrate salt ingestion determines the response.
    nutrient_topic
    Lithium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Lithium
    plain_language
    A sodium-coupled carrier links lithium to carbon metabolism.
    primary_references
    Human sodium-coupled citrate transporter, the orthologue of Drosophila Indy, as a novel target for lithium action. · 2003 · https://pubmed.ncbi.nlm.nih.gov/12826022/ · DOI 10.1042/BJ20030827

    Lithium: metal-sensitive enzymes, transport and cross-nutrient mechanisms (2026-09-19) · lines 264–270

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Expressed human transporter and human liver-cell experiments. · source_derived_draft · unverified_draft

    ## lithium-nact-human A sodium-coupled carrier links lithium to carbon metabolism. Lithium stimulated human NaCT-mediated citrate transport at concentrations relevant to prescription exposure. Model: Expressed human transporter and human liver-cell experiments. Limitations: Not evidence that trace lithium has the same effect or that citrate salt ingestion determines the response. Evidence access: Primary abstract Human sodium-coupled citrate transporter, the orthologue of Drosophila Indy, as a novel target for lithium action. · 2003 · https://pubmed.ncbi.nlm.nih.gov/12826022/ · DOI 10.1042/BJ20030827
    Complete structured claim and evidence

  3. F500W increased baseline transport but nearly eliminated additional lithium stimulation of human NaCT.

    Human SLC13A5 F500W variant → Human sodium-coupled citrate transporter / SLC13A5 source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Site-directed human transporter mutagenesis.
    limitations
    Engineered variant, not evidence of a common human nutritional phenotype.
    nutrient_topic
    Lithium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Lithium
    plain_language
    A protein variant can change responsiveness independently of intake.
    primary_references
    Species-specific influence of lithium on the activity of SLC13A5 (NaCT): lithium-induced activation is specific for the transporter in primates. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25617245/ · DOI 10.1124/jpet.114.221523
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Lithium: metal-sensitive enzymes, transport and cross-nutrient mechanisms (2026-09-19) · lines 296–302

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Site-directed human transporter mutagenesis. · source_derived_draft · unverified_draft

    ## lithium-nact-variant A protein variant can change responsiveness independently of intake. F500W increased baseline transport but nearly eliminated additional lithium stimulation of human NaCT. Model: Site-directed human transporter mutagenesis. Limitations: Engineered variant, not evidence of a common human nutritional phenotype. Evidence access: Primary abstract Species-specific influence of lithium on the activity of SLC13A5 (NaCT): lithium-induced activation is specific for the transporter in primates. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25617245/ · DOI 10.1124/jpet.114.221523
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards