Component

Lactose

Disaccharide included with calcium and phosphate in experimental mineral rescue diets.

3 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

Where it participates (unsigned role)

  1. The combined mineral/lactose rescue diet prevented rickets and osteomalacia in VDR-ablated mice.

    Inorganic phosphate → Skeletal matrix mineralization source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    Vitamin D–calcium–phosphate regulation.
    evidence_locator
    Abstract: reported experimental results
    evidence_scope
    D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison.
    experimental_model
    VDR-ablated mice and control littermates receiving a mineral/lactose rescue diet
    exposure
    Combined mineral/lactose rescue diet; individual ingredient contributions and exact formulation are not resolved by the retrieved abstract.
    limitations
    This is a combined dietary rescue of receptor-deficient mice, not phosphate monotherapy, not a D2/D3 trial, and not evidence that VDR has no direct skeletal functions.
    nutrient
    Vitamin D2 and D3 · Vitamin D2 and D3
    nutrient_topic
    Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3
    organism
    Mus musculus
    plain_language
    Improving mineral delivery protected the skeleton even when the vitamin D receptor was missing.
    primary_references
    [vdm-li1998] Normalization of mineral ion homeostasis by dietary means prevents hyperparathyroidism, rickets, and osteomalacia, but not alopecia in vitamin D receptor-ablated mice. (1998). https://pubmed.ncbi.nlm.nih.gov/9751523/ DOI: 10.1210/endo.139.10.6262
    tissue_or_cell_type
    Skeleton
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 761–775

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · VDR-ablated mice and control littermates receiving a mineral/lactose rescue diet · source_derived_draft · unverified_draft

    ### vdm-mineral-rescue-prevents-vdr-null-skeletal-defects The combined mineral/lactose rescue diet prevented rickets and osteomalacia in VDR-ablated mice. Condition category: machinery_impairment nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Improving mineral delivery protected the skeleton even when the vitamin D receptor was missing. organism: Mus musculus tissue_or_cell_type: Skeleton experimental_model: VDR-ablated mice and control littermates receiving a mineral/lactose rescue diet limitations: This is a combined dietary rescue of receptor-deficient mice, not phosphate monotherapy, not a D2/D3 trial, and not evidence that VDR has no direct skeletal functions. exposure: Combined mineral/lactose rescue diet; individual ingredient contributions and exact formulation are not resolved by the retrieved abstract. cross_nutrient: Vitamin D–calcium–phosphate regulation. evidence_locator: Abstract: reported experimental results nutrient: Vitamin D2 and D3 evidence_scope: D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison. [vdm-li1998] Normalization of mineral ion homeostasis by dietary means prevents hyperparathyroidism, rickets, and osteomalacia, but not alopecia in vitamin D receptor-ablated mice. (1998). https://pubmed.ncbi.nlm.nih.gov/9751523/ DOI: 10.1210/endo.139.10.6262
    Complete structured claim and evidence

  2. Mammary epithelial Tmem165 deletion reduced lactose biosynthesis in lactating mice.

    Mouse mammary epithelial TMEM165 loss → Mammary lactose biosynthesis source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    Mouse TMEM165 (affected_protein); Lactose (affected_product)
    evidence_span
    {"source_cache": "artifacts/manganese-glycosylation-sources/milk2019.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "88bcb50ecdb918803c5950bcff8f48665dbd17148b365a4f9f3b463fe7edd2a4", "start_char": 0, "end_char": 1462, "text_sha256": "88bcb50ecdb918803c5950bcff8f48665dbd17148b365a4f9f3b463fe7edd2a4", "text_characters": 1462}
    experimental_model
    Conditional mammary epithelial Tmem165 deletion in mice
    exposure
    Tissue-specific deletion with milk composition and pup-growth measurements.
    limitations
    The primary abstract supports normalized milk minerals and reduced lactose; altered concentration can reflect less milk dilution. Proposed cation/H+ exchange is an interpretation, not a transport stoichiometry measured here.
    nutrient_topic
    Manganese research collection; topical membership is not evidence of a direct dietary effect. · Manganese
    organism
    Mus musculus
    plain_language
    Manganese-handling machinery in the milk-producing cell affected milk production.
    primary_references
    [mn-gly-milk2019] Milk biosynthesis requires the Golgi cation exchanger TMEM165. (2019). https://pubmed.ncbi.nlm.nih.gov/30622138/ DOI: 10.1074/jbc.ra118.006270
    tissue_or_cell_type
    Lactating mammary gland and milk
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (2026-09-17) · lines 880–892

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Conditional mammary epithelial Tmem165 deletion in mice · source_derived_draft · unverified_draft

    ### mn-gly-mammary-lactose Mammary epithelial Tmem165 deletion reduced lactose biosynthesis in lactating mice. Condition category: machinery_impairment nutrient_topic: Manganese research collection; topical membership is not evidence of a direct dietary effect. plain_language: Manganese-handling machinery in the milk-producing cell affected milk production. organism: Mus musculus tissue_or_cell_type: Lactating mammary gland and milk experimental_model: Conditional mammary epithelial Tmem165 deletion in mice limitations: The primary abstract supports normalized milk minerals and reduced lactose; altered concentration can reflect less milk dilution. Proposed cation/H+ exchange is an interpretation, not a transport stoichiometry measured here. exposure: Tissue-specific deletion with milk composition and pup-growth measurements. cross_nutrient: Mouse TMEM165 (affected_protein); Lactose (affected_product) evidence_span: {"source_cache": "artifacts/manganese-glycosylation-sources/milk2019.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "88bcb50ecdb918803c5950bcff8f48665dbd17148b365a4f9f3b463fe7edd2a4", "start_char": 0, "end_char": 1462, "text_sha256": "88bcb50ecdb918803c5950bcff8f48665dbd17148b365a4f9f3b463fe7edd2a4", "text_characters": 1462} [mn-gly-milk2019] Milk biosynthesis requires the Golgi cation exchanger TMEM165. (2019). https://pubmed.ncbi.nlm.nih.gov/30622138/ DOI: 10.1074/jbc.ra118.006270
    Complete structured claim and evidence

  3. Pups nursed by mammary Tmem165-deficient dams had impaired growth.

    Mouse mammary epithelial TMEM165 loss → Growth of nursing mouse pups source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    Mouse TMEM165 (affected_protein); Lactose (affected_product)
    evidence_span
    {"source_cache": "artifacts/manganese-glycosylation-sources/milk2019.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "88bcb50ecdb918803c5950bcff8f48665dbd17148b365a4f9f3b463fe7edd2a4", "start_char": 0, "end_char": 1462, "text_sha256": "88bcb50ecdb918803c5950bcff8f48665dbd17148b365a4f9f3b463fe7edd2a4", "text_characters": 1462}
    experimental_model
    Conditional mammary epithelial Tmem165 deletion in mice
    exposure
    Tissue-specific deletion with milk composition and pup-growth measurements.
    limitations
    The primary abstract supports normalized milk minerals and reduced lactose; altered concentration can reflect less milk dilution. Proposed cation/H+ exchange is an interpretation, not a transport stoichiometry measured here.
    nutrient_topic
    Manganese research collection; topical membership is not evidence of a direct dietary effect. · Manganese
    organism
    Mus musculus
    plain_language
    The milk-producing-cell defect was accompanied by slower growth in nursing pups.
    primary_references
    [mn-gly-milk2019] Milk biosynthesis requires the Golgi cation exchanger TMEM165. (2019). https://pubmed.ncbi.nlm.nih.gov/30622138/ DOI: 10.1074/jbc.ra118.006270
    tissue_or_cell_type
    Lactating mammary gland and milk
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (2026-09-17) · lines 936–948

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Conditional mammary epithelial Tmem165 deletion in mice · source_derived_draft · unverified_draft

    ### mn-gly-mammary-pup-growth Pups nursed by mammary Tmem165-deficient dams had impaired growth. Condition category: machinery_impairment nutrient_topic: Manganese research collection; topical membership is not evidence of a direct dietary effect. plain_language: The milk-producing-cell defect was accompanied by slower growth in nursing pups. organism: Mus musculus tissue_or_cell_type: Lactating mammary gland and milk experimental_model: Conditional mammary epithelial Tmem165 deletion in mice limitations: The primary abstract supports normalized milk minerals and reduced lactose; altered concentration can reflect less milk dilution. Proposed cation/H+ exchange is an interpretation, not a transport stoichiometry measured here. exposure: Tissue-specific deletion with milk composition and pup-growth measurements. cross_nutrient: Mouse TMEM165 (affected_protein); Lactose (affected_product) evidence_span: {"source_cache": "artifacts/manganese-glycosylation-sources/milk2019.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "88bcb50ecdb918803c5950bcff8f48665dbd17148b365a4f9f3b463fe7edd2a4", "start_char": 0, "end_char": 1462, "text_sha256": "88bcb50ecdb918803c5950bcff8f48665dbd17148b365a4f9f3b463fe7edd2a4", "text_characters": 1462} [mn-gly-milk2019] Milk biosynthesis requires the Golgi cation exchanger TMEM165. (2019). https://pubmed.ncbi.nlm.nih.gov/30622138/ DOI: 10.1074/jbc.ra118.006270
    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