Component

Mouse Slc23a1 gene

Mouse gene encoding SVCT1; distinct from its protein. The SVCT2 gene was historically called Slc23a1 in Sotiriou 2002.

5 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. Pups born to Slc23a1-null dams had approximately 45% perinatal mortality, including heterozygous and homozygous-null pups.

    Mouse Slc23a1 gene → Perinatal survival source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Slc23a1 knockout mice and wild-type controls
    exposure
    Breeding Slc23a1-null dams
    limitations
    Genotype of dam and pup must be distinguished; this does not define human pregnancy requirements.
    nutrient_topic
    Vitamin C research collection; topical membership is not evidence of a direct dietary effect. · Vitamin C
    organism
    Mus musculus
    plain_language
    Maternal loss of the renal vitamin C transporter threatened newborn survival.
    primary_references
    [corpe2010] Vitamin C transporter Slc23a1 links renal reabsorption, vitamin C tissue accumulation, and perinatal survival in mice. (2010). https://pubmed.ncbi.nlm.nih.gov/20200446/ DOI: 10.1172/jci39191
    tissue_or_cell_type
    Maternal-fetal system
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 169–180

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Slc23a1 knockout mice and wild-type controls · source_derived_draft · unverified_draft

    ### vc-transport-svct1-maternal-survival Pups born to Slc23a1-null dams had approximately 45% perinatal mortality, including heterozygous and homozygous-null pups. Condition category: machinery_impairment nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: Maternal loss of the renal vitamin C transporter threatened newborn survival. organism: Mus musculus tissue_or_cell_type: Maternal-fetal system experimental_model: Slc23a1 knockout mice and wild-type controls limitations: Genotype of dam and pup must be distinguished; this does not define human pregnancy requirements. exposure: Breeding Slc23a1-null dams cross_nutrient: false [corpe2010] Vitamin C transporter Slc23a1 links renal reabsorption, vitamin C tissue accumulation, and perinatal survival in mice. (2010). https://pubmed.ncbi.nlm.nih.gov/20200446/ DOI: 10.1172/jci39191
    Complete structured claim and evidence

  2. Plasma ascorbate was approximately 50–70% lower in Slc23a1-null mice than wild-type mice.

    Mouse Slc23a1 gene → Plasma ascorbate concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Slc23a1 knockout mice and wild-type controls
    exposure
    Slc23a1 knockout versus wild type
    limitations
    Mouse concentration phenotype; do not use as a human deficiency threshold.
    nutrient_topic
    Vitamin C research collection; topical membership is not evidence of a direct dietary effect. · Vitamin C
    organism
    Mus musculus
    plain_language
    Renal vitamin C wasting lowered circulating vitamin C in these mice.
    primary_references
    [corpe2010] Vitamin C transporter Slc23a1 links renal reabsorption, vitamin C tissue accumulation, and perinatal survival in mice. (2010). https://pubmed.ncbi.nlm.nih.gov/20200446/ DOI: 10.1172/jci39191
    tissue_or_cell_type
    Plasma
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 156–167

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Slc23a1 knockout mice and wild-type controls · source_derived_draft · unverified_draft

    ### vc-transport-svct1-plasma Plasma ascorbate was approximately 50–70% lower in Slc23a1-null mice than wild-type mice. Condition category: machinery_impairment nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: Renal vitamin C wasting lowered circulating vitamin C in these mice. organism: Mus musculus tissue_or_cell_type: Plasma experimental_model: Slc23a1 knockout mice and wild-type controls limitations: Mouse concentration phenotype; do not use as a human deficiency threshold. exposure: Slc23a1 knockout versus wild type cross_nutrient: false [corpe2010] Vitamin C transporter Slc23a1 links renal reabsorption, vitamin C tissue accumulation, and perinatal survival in mice. (2010). https://pubmed.ncbi.nlm.nih.gov/20200446/ DOI: 10.1172/jci39191
    Complete structured claim and evidence

  3. Slc23a1 deletion raised renal ascorbate fractional excretion about 16–18-fold in female mice and 6–7-fold in males; female reabsorption was essentially abolished.

    Mouse Slc23a1 gene → Renal ascorbate fractional excretion source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Slc23a1 knockout mice and wild-type controls
    exposure
    Slc23a1 knockout versus wild type
    limitations
    Sex-specific renal clearances; inulin clearance was unchanged. This is transporter loss, not low intake.
    nutrient_topic
    Vitamin C research collection; topical membership is not evidence of a direct dietary effect. · Vitamin C
    organism
    Mus musculus
    plain_language
    Removing SVCT1 made mice lose more filtered vitamin C in urine.
    primary_references
    [corpe2010] Vitamin C transporter Slc23a1 links renal reabsorption, vitamin C tissue accumulation, and perinatal survival in mice. (2010). https://pubmed.ncbi.nlm.nih.gov/20200446/ DOI: 10.1172/jci39191
    tissue_or_cell_type
    Kidney
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 143–154

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Slc23a1 knockout mice and wild-type controls · source_derived_draft · unverified_draft

    ### vc-transport-svct1-renal-loss Slc23a1 deletion raised renal ascorbate fractional excretion about 16–18-fold in female mice and 6–7-fold in males; female reabsorption was essentially abolished. Condition category: machinery_impairment nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing SVCT1 made mice lose more filtered vitamin C in urine. organism: Mus musculus tissue_or_cell_type: Kidney experimental_model: Slc23a1 knockout mice and wild-type controls limitations: Sex-specific renal clearances; inulin clearance was unchanged. This is transporter loss, not low intake. exposure: Slc23a1 knockout versus wild type cross_nutrient: false [corpe2010] Vitamin C transporter Slc23a1 links renal reabsorption, vitamin C tissue accumulation, and perinatal survival in mice. (2010). https://pubmed.ncbi.nlm.nih.gov/20200446/ DOI: 10.1172/jci39191
    Complete structured claim and evidence

  4. Slc23a1-null mice increased endogenous ascorbate synthesis despite losing as much as 70% of their body ascorbate stores in urine daily.

    Mouse Slc23a1 gene → Ascorbate biosynthesis source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Slc23a1 knockout mice and wild-type controls
    exposure
    Slc23a1 knockout
    limitations
    Compensation depends on intact murine biosynthesis; humans cannot be assumed to compensate this way.
    nutrient_topic
    Vitamin C research collection; topical membership is not evidence of a direct dietary effect. · Vitamin C
    organism
    Mus musculus
    plain_language
    These mice could partly compensate for urinary loss by making more vitamin C.
    primary_references
    [corpe2010] Vitamin C transporter Slc23a1 links renal reabsorption, vitamin C tissue accumulation, and perinatal survival in mice. (2010). https://pubmed.ncbi.nlm.nih.gov/20200446/ DOI: 10.1172/jci39191
    tissue_or_cell_type
    Whole body/liver
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 195–206

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Slc23a1 knockout mice and wild-type controls · source_derived_draft · unverified_draft

    ### vc-transport-svct1-synthesis-compensation Slc23a1-null mice increased endogenous ascorbate synthesis despite losing as much as 70% of their body ascorbate stores in urine daily. Condition category: machinery_impairment nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: These mice could partly compensate for urinary loss by making more vitamin C. organism: Mus musculus tissue_or_cell_type: Whole body/liver experimental_model: Slc23a1 knockout mice and wild-type controls limitations: Compensation depends on intact murine biosynthesis; humans cannot be assumed to compensate this way. exposure: Slc23a1 knockout cross_nutrient: false [corpe2010] Vitamin C transporter Slc23a1 links renal reabsorption, vitamin C tissue accumulation, and perinatal survival in mice. (2010). https://pubmed.ncbi.nlm.nih.gov/20200446/ DOI: 10.1172/jci39191
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Providing Slc23a1-null pregnant mice 330 mg/L ascorbate in drinking water from mating to delivery prevented the excess perinatal mortality of their null offspring.

    L-Ascorbate → Perinatal survival source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Slc23a1 knockout mice and wild-type controls
    exposure
    Slc23a1-null dams; 330 mg/L drinking-water ascorbate during pregnancy
    limitations
    Animal rescue dose; not a human dosing recommendation or correction of the deleted transporter.
    nutrient_topic
    Vitamin C research collection; topical membership is not evidence of a direct dietary effect. · Vitamin C
    organism
    Mus musculus
    plain_language
    Additional vitamin C rescued survival in this maternal transporter-loss model.
    primary_references
    [corpe2010] Vitamin C transporter Slc23a1 links renal reabsorption, vitamin C tissue accumulation, and perinatal survival in mice. (2010). https://pubmed.ncbi.nlm.nih.gov/20200446/ DOI: 10.1172/jci39191
    tissue_or_cell_type
    Maternal-fetal system
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 182–193

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Slc23a1 knockout mice and wild-type controls · source_derived_draft · unverified_draft

    ### vc-transport-svct1-maternal-rescue Providing Slc23a1-null pregnant mice 330 mg/L ascorbate in drinking water from mating to delivery prevented the excess perinatal mortality of their null offspring. Condition category: machinery_impairment nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: Additional vitamin C rescued survival in this maternal transporter-loss model. organism: Mus musculus tissue_or_cell_type: Maternal-fetal system experimental_model: Slc23a1 knockout mice and wild-type controls limitations: Animal rescue dose; not a human dosing recommendation or correction of the deleted transporter. exposure: Slc23a1-null dams; 330 mg/L drinking-water ascorbate during pregnancy cross_nutrient: false [corpe2010] Vitamin C transporter Slc23a1 links renal reabsorption, vitamin C tissue accumulation, and perinatal survival in mice. (2010). https://pubmed.ncbi.nlm.nih.gov/20200446/ DOI: 10.1172/jci39191
    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