Component

Intestinal cobalamin absorption

Intestinal cobalamin absorption

6 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 acts on it

  1. Mapping and sequencing identified two independent disease-specific CUBN mutations across 17 Finnish families with selective intestinal cobalamin malabsorption.

    Human biallelic CUBN disease genotypes in Aminoff 1999 → Intestinal cobalamin absorption source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    17 Finnish MGA1 families; linkage and molecular analysis
    exposure
    Inherited biallelic CUBN disease genotypes
    limitations
    Family-genetic evidence; allele-specific biochemical steps require separate functional experiments.
    nutrient_topic
    Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B12 (cobalamins)
    organism
    Homo sapiens
    plain_language
    Inherited cubilin defects can block B12 absorption.
    primary_references
    [aminoff-1999-cubn] Mutations in CUBN, encoding the intrinsic factor-vitamin B12 receptor, cubilin, cause hereditary megaloblastic anaemia 1. (1999). https://pubmed.ncbi.nlm.nih.gov/10080186/ DOI: 10.1038/6831
    tissue_or_cell_type
    Small-intestinal absorption
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin B12: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 283–294

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · 17 Finnish MGA1 families; linkage and molecular analysis · source_derived_draft · unverified_draft

    ### b12-abs-cubn-genetic-malabsorption Mapping and sequencing identified two independent disease-specific CUBN mutations across 17 Finnish families with selective intestinal cobalamin malabsorption. Condition category: machinery_impairment nutrient_topic: Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Inherited cubilin defects can block B12 absorption. organism: Homo sapiens tissue_or_cell_type: Small-intestinal absorption experimental_model: 17 Finnish MGA1 families; linkage and molecular analysis limitations: Family-genetic evidence; allele-specific biochemical steps require separate functional experiments. exposure: Inherited biallelic CUBN disease genotypes cross_nutrient: false [aminoff-1999-cubn] Mutations in CUBN, encoding the intrinsic factor-vitamin B12 receptor, cubilin, cause hereditary megaloblastic anaemia 1. (1999). https://pubmed.ncbi.nlm.nih.gov/10080186/ DOI: 10.1038/6831
    Complete structured claim and evidence

  2. Biallelic GIF mutations in seven families with juvenile cobalamin deficiency identified inherited intrinsic-factor deficiency in cases initially suspected to have receptor-mediated IGS.

    Human biallelic GIF disease genotypes in Tanner 2005 → Intestinal cobalamin absorption source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Human family linkage and sequencing study
    exposure
    Inherited GIF variants
    limitations
    Genetic classification; not evidence that all variants or all malabsorption have the same cause. Earlier absorption tests were inconclusive.
    nutrient_topic
    Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B12 (cobalamins)
    organism
    Homo sapiens
    plain_language
    Some inherited absorption failures originate in intrinsic factor.
    primary_references
    [tanner-2005-gif] Hereditary juvenile cobalamin deficiency caused by mutations in the intrinsic factor gene. (2005). https://pubmed.ncbi.nlm.nih.gov/15738392/ DOI: 10.1073/pnas.0500517102
    tissue_or_cell_type
    Gastric intrinsic factor/intestinal absorption pathway
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin B12: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 309–320

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human family linkage and sequencing study · source_derived_draft · unverified_draft

    ### b12-abs-gif-genetic-malabsorption Biallelic GIF mutations in seven families with juvenile cobalamin deficiency identified inherited intrinsic-factor deficiency in cases initially suspected to have receptor-mediated IGS. Condition category: machinery_impairment nutrient_topic: Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Some inherited absorption failures originate in intrinsic factor. organism: Homo sapiens tissue_or_cell_type: Gastric intrinsic factor/intestinal absorption pathway experimental_model: Human family linkage and sequencing study limitations: Genetic classification; not evidence that all variants or all malabsorption have the same cause. Earlier absorption tests were inconclusive. exposure: Inherited GIF variants cross_nutrient: false [tanner-2005-gif] Hereditary juvenile cobalamin deficiency caused by mutations in the intrinsic factor gene. (2005). https://pubmed.ncbi.nlm.nih.gov/15738392/ DOI: 10.1073/pnas.0500517102
    Complete structured claim and evidence

  3. Type II antibodies prevented absorption in pernicious-anemia patients when added to a preformed intrinsic-factor-B12 complex.

    Human type II intrinsic-factor binding autoantibodies → Intestinal cobalamin absorption source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Human absorption experiments with preassembled IF-B12
    exposure
    IF plus B12 followed by type II antibody
    limitations
    Demonstrates impaired absorption; does not identify an epitope or directly prove contact competition at cubilin.
    nutrient_topic
    Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B12 (cobalamins)
    organism
    Homo sapiens
    plain_language
    Other antibodies interfered even after B12 had bound its carrier.
    primary_references
    [schade-1967-if-antibody] Studies on antibody to intrinsic factor. (1967). https://pubmed.ncbi.nlm.nih.gov/6021209/ DOI: 10.1172/jci105563
    tissue_or_cell_type
    Intestinal intrinsic-factor-dependent absorption
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin B12: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 517–528

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human absorption experiments with preassembled IF-B12 · source_derived_draft · unverified_draft

    ### b12-abs-if-antibody-preformed-complex Type II antibodies prevented absorption in pernicious-anemia patients when added to a preformed intrinsic-factor-B12 complex. Condition category: machinery_impairment nutrient_topic: Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Other antibodies interfered even after B12 had bound its carrier. organism: Homo sapiens tissue_or_cell_type: Intestinal intrinsic-factor-dependent absorption experimental_model: Human absorption experiments with preassembled IF-B12 limitations: Demonstrates impaired absorption; does not identify an epitope or directly prove contact competition at cubilin. exposure: IF plus B12 followed by type II antibody cross_nutrient: false [schade-1967-if-antibody] Studies on antibody to intrinsic factor. (1967). https://pubmed.ncbi.nlm.nih.gov/6021209/ DOI: 10.1172/jci105563
    Complete structured claim and evidence

  4. In three patients with pancreatic insufficiency, oral cobinamide 100 nmol corrected malabsorption of 0.4 nmol radiocobalamin in Schilling tests, comparably to trypsin.

    Cobinamide → Intestinal cobalamin absorption source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Three human pancreatic-insufficiency patients and parallel human binding assays
    exposure
    Cobinamide competitor during Schilling test
    limitations
    Small physiological intervention; cobinamide is an experimental analogue, not B12 nutrition. The absorption defect was pancreatic machinery impairment.
    nutrient_topic
    Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B12 (cobalamins)
    organism
    Homo sapiens
    plain_language
    Blocking haptocorrin competition restored tracer absorption in three patients.
    primary_references
    [allen-1978-cobinamide] Correction of cobalamin malabsorption in pancreatic insufficiency with a cobalamin analogue that binds with high affinity to R protein but not to intrinsic factor. In vivo evidence that a failure to partially degrade R protein is responsible for cobalamin malabsorption in pancreatic insufficiency. (1978). https://pubmed.ncbi.nlm.nih.gov/659618/ DOI: 10.1172/jci109083
    tissue_or_cell_type
    Intestinal absorption and urinary radiotracer recovery
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin B12: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 205–216

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Three human pancreatic-insufficiency patients and parallel human binding assays · source_derived_draft · unverified_draft

    ### b12-abs-pancreatic-competitor-rescue In three patients with pancreatic insufficiency, oral cobinamide 100 nmol corrected malabsorption of 0.4 nmol radiocobalamin in Schilling tests, comparably to trypsin. Condition category: machinery_impairment nutrient_topic: Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Blocking haptocorrin competition restored tracer absorption in three patients. organism: Homo sapiens tissue_or_cell_type: Intestinal absorption and urinary radiotracer recovery experimental_model: Three human pancreatic-insufficiency patients and parallel human binding assays limitations: Small physiological intervention; cobinamide is an experimental analogue, not B12 nutrition. The absorption defect was pancreatic machinery impairment. exposure: Cobinamide competitor during Schilling test cross_nutrient: false [allen-1978-cobinamide] Correction of cobalamin malabsorption in pancreatic insufficiency with a cobalamin analogue that binds with high affinity to R protein but not to intrinsic factor. In vivo evidence that a failure to partially degrade R protein is responsible for cobalamin malabsorption in pancreatic insufficiency. (1978). https://pubmed.ncbi.nlm.nih.gov/659618/ DOI: 10.1172/jci109083
    Complete structured claim and evidence

  5. Vitamin B12 malabsorption was most prominent in patients on metformin, and pathological Schilling tests, increased glycocholic acid deconjugation and decreased faecal bile acid excretion normalised or improved after stopping the biguanide or giving antibiotics, suggesting small-intestinal bacterial overgrowth binding the intrinsic-factor-B12 complex.

    Metformin → Intestinal cobalamin absorption source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/metformin-research/873086.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1889488dcc83ec22842eccf766b842761a6c10643dbf7d8e6f8308331dfdf01c", "start_char": 0, "end_char": 1442, "text_sha256": "1889488dcc83ec22842eccf766b842761a6c10643dbf7d8e6f8308331dfdf01c"}
    experimental_model
    Breath test, faecal bile acid measurement and Schilling tests in maturity-onset diabetics on biguanides
    exposure
    Phenformin, buformin or metformin, with antibiotic treatment as a test
    limitations
    A 1977 study using the Schilling test. It proposes bacterial overgrowth as the mechanism; the antibiotic reversal is suggestive rather than definitive, and it competes with the calcium-dependent explanation.
    nutrient_topic
    Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. · Metformin
    organism
    Human
    plain_language
    A second explanation: bacteria in the small bowel take up the vitamin before the body can.
    primary_references
    [metformin-p873086] Alteration of bile acid metabolism and vitamin-B12-absorption in diabetics on biguanides. (1977). https://pubmed.ncbi.nlm.nih.gov/873086/ DOI: 10.1007/bf01219698
    tissue_or_cell_type
    Small intestine
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 1165–1176

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Breath test, faecal bile acid measurement and Schilling tests in maturity-onset diabetics on biguanides · source_derived_draft · unverified_draft

    ### metformin-b12-bacterial-overgrowth Vitamin B12 malabsorption was most prominent in patients on metformin, and pathological Schilling tests, increased glycocholic acid deconjugation and decreased faecal bile acid excretion normalised or improved after stopping the biguanide or giving antibiotics, suggesting small-intestinal bacterial overgrowth binding the intrinsic-factor-B12 complex. Condition category: nutrient_deficiency nutrient_topic: Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. plain_language: A second explanation: bacteria in the small bowel take up the vitamin before the body can. organism: Human tissue_or_cell_type: Small intestine experimental_model: Breath test, faecal bile acid measurement and Schilling tests in maturity-onset diabetics on biguanides limitations: A 1977 study using the Schilling test. It proposes bacterial overgrowth as the mechanism; the antibiotic reversal is suggestive rather than definitive, and it competes with the calcium-dependent explanation. exposure: Phenformin, buformin or metformin, with antibiotic treatment as a test evidence_span: {"source_cache": "artifacts/metformin-research/873086.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1889488dcc83ec22842eccf766b842761a6c10643dbf7d8e6f8308331dfdf01c", "start_char": 0, "end_char": 1442, "text_sha256": "1889488dcc83ec22842eccf766b842761a6c10643dbf7d8e6f8308331dfdf01c"} [metformin-p873086] Alteration of bile acid metabolism and vitamin-B12-absorption in diabetics on biguanides. (1977). https://pubmed.ncbi.nlm.nih.gov/873086/ DOI: 10.1007/bf01219698
    Complete structured claim and evidence

  6. The authors attributed diminished B12 absorption and low serum B12 and transcobalamin-bound B12 during metformin to a calcium-dependent ileal membrane antagonism, since uptake of the B12-intrinsic factor complex by ileal cell surface receptors is calcium-dependent.

    Metformin → Intestinal cobalamin absorption source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/metformin-research/10977010.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7aed1bfb7ee680b248e083db467fd4a8199ac933e8a12b4c6ba08f9931a7794b", "start_char": 0, "end_char": 1267, "text_sha256": "7aed1bfb7ee680b248e083db467fd4a8199ac933e8a12b4c6ba08f9931a7794b"}
    experimental_model
    Comparative study in 21 people with type 2 diabetes, 14 switched to metformin, with oral calcium supplementation
    exposure
    Metformin for three months, then oral calcium supplementation
    limitations
    A small, non-randomised comparative study. The calcium-dependent ileal mechanism is the authors’ interpretation of the reversal, not a direct measurement of receptor binding.
    nutrient_topic
    Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. · Metformin
    organism
    Human
    plain_language
    The proposed step is the calcium-dependent grab of the vitamin at the ileal cell surface.
    primary_references
    [metformin-p10977010] Increased intake of calcium reverses vitamin B12 malabsorption induced by metformin. (2000). https://pubmed.ncbi.nlm.nih.gov/10977010/ DOI: 10.2337/diacare.23.9.1227
    tissue_or_cell_type
    Ileal absorption
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 1152–1163

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Comparative study in 21 people with type 2 diabetes, 14 switched to metformin, with oral calcium supplementation · source_derived_draft · unverified_draft

    ### metformin-b12-calcium-mechanism The authors attributed diminished B12 absorption and low serum B12 and transcobalamin-bound B12 during metformin to a calcium-dependent ileal membrane antagonism, since uptake of the B12-intrinsic factor complex by ileal cell surface receptors is calcium-dependent. Condition category: nutrient_deficiency nutrient_topic: Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. plain_language: The proposed step is the calcium-dependent grab of the vitamin at the ileal cell surface. organism: Human tissue_or_cell_type: Ileal absorption experimental_model: Comparative study in 21 people with type 2 diabetes, 14 switched to metformin, with oral calcium supplementation limitations: A small, non-randomised comparative study. The calcium-dependent ileal mechanism is the authors’ interpretation of the reversal, not a direct measurement of receptor binding. exposure: Metformin for three months, then oral calcium supplementation evidence_span: {"source_cache": "artifacts/metformin-research/10977010.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7aed1bfb7ee680b248e083db467fd4a8199ac933e8a12b4c6ba08f9931a7794b", "start_char": 0, "end_char": 1267, "text_sha256": "7aed1bfb7ee680b248e083db467fd4a8199ac933e8a12b4c6ba08f9931a7794b"} [metformin-p10977010] Increased intake of calcium reverses vitamin B12 malabsorption induced by metformin. (2000). https://pubmed.ncbi.nlm.nih.gov/10977010/ DOI: 10.2337/diacare.23.9.1227
    Complete structured claim and evidence

In the sources

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