Component

Mouse insulin receptor / Insr

Mouse insulin receptor / Insr. Species, exposure and limitations are retained in each linked 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 acts on it

  1. GPX1-overexpressing mice showed reduced insulin-stimulated receptor phosphorylation in liver and Akt phosphorylation in liver and soleus.

    Mouse Gpx1 overexpression genotype → Mouse insulin receptor / Insr source_derived_draftungraded
    Experimental context and source evidence
    curation_topic
    selenium · Selenium
    experimental_condition
    Wild-type mice on the same diet GPX1 overexpression · Mouse Gpx1 overexpression genotype Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_contrast
    {"intervention": "GPX1 overexpression", "comparator": "Wild-type mice on the same diet", "endpoint": "Insulin-stimulated phosphorylation", "effect_direction": "decrease", "combination": "single", "conditions": [{"entity_slug": "mouse-gpx1-overexpression", "state": "GPX1 overexpression"}]} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Male transgenic mice; selenium-adequate 0.4 mg/kg diet, ages 8 to 24 weeks
    limitations
    Overexpression experiment, not dietary selenium excess. Excess ROS quenching is a proposed explanation rather than a measured universal mechanism.
    primary_references
    McClung et al. 2004; DOI:10.1073/pnas.0308096101; PMID:15184668; https://pmc.ncbi.nlm.nih.gov/articles/PMC428436/

    Diabetes cascade: targeted primary-source supplement · lines 30–30

    See claim-local references; curated paraphrases reviewed 2026-09-20. · supports · Male transgenic mice; selenium-adequate 0.4 mg/kg diet, ages 8 to 24 weeks · source_derived_draft · unverified_draft

    GPX1-overexpressing mice showed reduced insulin-stimulated receptor phosphorylation in liver and Akt phosphorylation in liver and soleus. Model: Male transgenic mice; selenium-adequate 0.4 mg/kg diet, ages 8 to 24 weeks. Limits: Overexpression experiment, not dietary selenium excess. Excess ROS quenching is a proposed explanation rather than a measured universal mechanism. Primary reference: McClung et al. 2004; DOI:10.1073/pnas.0308096101; PMID:15184668; https://pmc.ncbi.nlm.nih.gov/articles/PMC428436/
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Chromium-associated GLUT4 trafficking in this study was not accompanied by enhancement of the examined insulin-receptor, IRS-1, PI3K or Akt signaling steps.

    Chromium(III) picolinate / CrPic → Insulin receptor autophosphorylation source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/chromium-research/16339278.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "57c07800ec80a0386c1c510fe0bd73bc5ebf196541580a5255565f8deafde657", "start_char": 0, "end_char": 1949, "text_sha256": "57c07800ec80a0386c1c510fe0bd73bc5ebf196541580a5255565f8deafde657"}
    experimental_model
    GLUT4 trafficking, glucose uptake and cholesterol add-back experiments
    exposure
    Chromium(III) chloride or chromium picolinate; insulin stimulation and cholesterol manipulation
    limitations
    Cell-culture pharmacology does not establish an essential dietary function. Vesicle arrival near the membrane and actual membrane insertion are different observations; no amplification of the tested proximal insulin signals was found.
    nutrient_topic
    Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
    organism
    Mouse 3T3-L1 adipocytes
    plain_language
    The transporter effect did not require a bigger response in the insulin-signaling measurements tested here.
    primary_references
    [chromium-p16339278] Chromium activates glucose transporter 4 trafficking and enhances insulin-stimulated glucose transport in 3T3-L1 adipocytes via a cholesterol-dependent mechanism. (2006). https://pubmed.ncbi.nlm.nih.gov/16339278/ DOI: 10.1210/me.2005-0255
    tissue_or_cell_type
    Cultured adipocyte plasma membrane

    Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 341–352

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · GLUT4 trafficking, glucose uptake and cholesterol add-back experiments · source_derived_draft · unverified_draft

    ### chromium-proximal-signaling-not-amplified Chromium-associated GLUT4 trafficking in this study was not accompanied by enhancement of the examined insulin-receptor, IRS-1, PI3K or Akt signaling steps. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The transporter effect did not require a bigger response in the insulin-signaling measurements tested here. organism: Mouse 3T3-L1 adipocytes tissue_or_cell_type: Cultured adipocyte plasma membrane experimental_model: GLUT4 trafficking, glucose uptake and cholesterol add-back experiments limitations: Cell-culture pharmacology does not establish an essential dietary function. Vesicle arrival near the membrane and actual membrane insertion are different observations; no amplification of the tested proximal insulin signals was found. exposure: Chromium(III) chloride or chromium picolinate; insulin stimulation and cholesterol manipulation evidence_span: {"source_cache": "artifacts/chromium-research/16339278.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "57c07800ec80a0386c1c510fe0bd73bc5ebf196541580a5255565f8deafde657", "start_char": 0, "end_char": 1949, "text_sha256": "57c07800ec80a0386c1c510fe0bd73bc5ebf196541580a5255565f8deafde657"} [chromium-p16339278] Chromium activates glucose transporter 4 trafficking and enhances insulin-stimulated glucose transport in 3T3-L1 adipocytes via a cholesterol-dependent mechanism. (2006). https://pubmed.ncbi.nlm.nih.gov/16339278/ DOI: 10.1210/me.2005-0255
    Complete structured claim and evidence

  2. Lipoic acid increased glucose uptake in 3T3-L1 adipocytes; intracellular thiol modification or inhibition of the upstream oxidant response blocked stimulation.

    Lipoic acid → Mouse adipocyte glucose uptake source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/ala-research/12948866.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0440cb8edaf0213af3824367ee799d1a1916ed2340c9da99588d83c7581804b9", "start_char": 0, "end_char": 1489, "text_sha256": "0440cb8edaf0213af3824367ee799d1a1916ed2340c9da99588d83c7581804b9"}
    experimental_model
    Protein-thiol, phosphorylation and glucose-uptake assays
    exposure
    Alpha-lipoic-acid stimulation with redox/thiol inhibitors
    limitations
    Cell-culture redox signaling; not proof that lipoic acid invariably lowers oxidation in all settings.
    nutrient_topic
    Alpha-lipoic acid research collection; topical membership is not evidence of a direct dietary effect. · Lipoic acid
    organism
    Mouse
    plain_language
    The glucose response depended on the cell’s redox-signaling machinery.
    primary_references
    [ala-p12948866] Alpha-lipoic acid decreases thiol reactivity of the insulin receptor and protein tyrosine phosphatase 1B in 3T3-L1 adipocytes. (2003). https://pubmed.ncbi.nlm.nih.gov/12948866/ DOI: 10.1016/s0006-2952(03)00395-2
    tissue_or_cell_type
    3T3-L1 adipocytes

    Alpha-lipoic acid: cofactor assembly, redox signaling and nutrient interactions (2026-09-17) · lines 962–973

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Protein-thiol, phosphorylation and glucose-uptake assays · source_derived_draft · unverified_draft

    ### ala-adipocyte-glucose Lipoic acid increased glucose uptake in 3T3-L1 adipocytes; intracellular thiol modification or inhibition of the upstream oxidant response blocked stimulation. Condition category: normal nutrient_topic: Alpha-lipoic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: The glucose response depended on the cell’s redox-signaling machinery. organism: Mouse tissue_or_cell_type: 3T3-L1 adipocytes experimental_model: Protein-thiol, phosphorylation and glucose-uptake assays limitations: Cell-culture redox signaling; not proof that lipoic acid invariably lowers oxidation in all settings. exposure: Alpha-lipoic-acid stimulation with redox/thiol inhibitors evidence_span: {"source_cache": "artifacts/ala-research/12948866.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0440cb8edaf0213af3824367ee799d1a1916ed2340c9da99588d83c7581804b9", "start_char": 0, "end_char": 1489, "text_sha256": "0440cb8edaf0213af3824367ee799d1a1916ed2340c9da99588d83c7581804b9"} [ala-p12948866] Alpha-lipoic acid decreases thiol reactivity of the insulin receptor and protein tyrosine phosphatase 1B in 3T3-L1 adipocytes. (2003). https://pubmed.ncbi.nlm.nih.gov/12948866/ DOI: 10.1016/s0006-2952(03)00395-2
    Complete structured claim and evidence

  3. Lipoic-acid treatment increased intracellular oxidant signals, reduced insulin-receptor thiol reactivity and increased receptor phosphorylation.

    Lipoic acid → Mouse adipocyte insulin-receptor autophosphorylation source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/ala-research/12948866.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0440cb8edaf0213af3824367ee799d1a1916ed2340c9da99588d83c7581804b9", "start_char": 0, "end_char": 1489, "text_sha256": "0440cb8edaf0213af3824367ee799d1a1916ed2340c9da99588d83c7581804b9"}
    experimental_model
    Protein-thiol, phosphorylation and glucose-uptake assays
    exposure
    Alpha-lipoic-acid stimulation with redox/thiol inhibitors
    limitations
    Cell-culture redox signaling; not proof that lipoic acid invariably lowers oxidation in all settings.
    nutrient_topic
    Alpha-lipoic acid research collection; topical membership is not evidence of a direct dietary effect. · Lipoic acid
    organism
    Mouse
    plain_language
    A local oxidant signal accompanied insulin-receptor activation.
    primary_references
    [ala-p12948866] Alpha-lipoic acid decreases thiol reactivity of the insulin receptor and protein tyrosine phosphatase 1B in 3T3-L1 adipocytes. (2003). https://pubmed.ncbi.nlm.nih.gov/12948866/ DOI: 10.1016/s0006-2952(03)00395-2
    tissue_or_cell_type
    3T3-L1 adipocytes

    Alpha-lipoic acid: cofactor assembly, redox signaling and nutrient interactions (2026-09-17) · lines 936–947

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Protein-thiol, phosphorylation and glucose-uptake assays · source_derived_draft · unverified_draft

    ### ala-adipocyte-insr-redox Lipoic-acid treatment increased intracellular oxidant signals, reduced insulin-receptor thiol reactivity and increased receptor phosphorylation. Condition category: normal nutrient_topic: Alpha-lipoic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: A local oxidant signal accompanied insulin-receptor activation. organism: Mouse tissue_or_cell_type: 3T3-L1 adipocytes experimental_model: Protein-thiol, phosphorylation and glucose-uptake assays limitations: Cell-culture redox signaling; not proof that lipoic acid invariably lowers oxidation in all settings. exposure: Alpha-lipoic-acid stimulation with redox/thiol inhibitors evidence_span: {"source_cache": "artifacts/ala-research/12948866.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0440cb8edaf0213af3824367ee799d1a1916ed2340c9da99588d83c7581804b9", "start_char": 0, "end_char": 1489, "text_sha256": "0440cb8edaf0213af3824367ee799d1a1916ed2340c9da99588d83c7581804b9"} [ala-p12948866] Alpha-lipoic acid decreases thiol reactivity of the insulin receptor and protein tyrosine phosphatase 1B in 3T3-L1 adipocytes. (2003). https://pubmed.ncbi.nlm.nih.gov/12948866/ DOI: 10.1016/s0006-2952(03)00395-2
    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