Component
Insulin receptor autophosphorylation
Independent biological entity. Read linked claims for experimental scope and context.
2 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What acts on it
Insulin receptor autophosphorylation was reduced about 50% in muscle preparations from Mg-deficient rats, despite similar insulin binding.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- cross_nutrient
- Magnesium -> insulin signaling -> carbohydrate handling.
- experimental_model
- Partially purified rat gastrocnemius receptors.
- limitations
- A depletion experiment; not isolated Mg binding to a particular receptor site.
- nutrient_topic
- Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
- organism
- Rattus norvegicus
- plain_language
- The receptor could still bind insulin, but its downstream activation was impaired.
- primary_references
- [mg-suarez1995] Impaired tyrosine-kinase activity of muscle insulin receptors from hypomagnesaemic rats (1995). https://pubmed.ncbi.nlm.nih.gov/8582534/ DOI: 10.1007/bf00401757
- tissue_or_cell_type
- Rat gastrocnemius receptor preparations and perfused hindquarter
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1503–1513
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Partially purified rat gastrocnemius receptors. · source_derived_draft · unverified_draft
### mg-deficiency-insr-autophosphorylation Insulin receptor autophosphorylation was reduced about 50% in muscle preparations from Mg-deficient rats, despite similar insulin binding. Condition category: nutrient_deficiency nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The receptor could still bind insulin, but its downstream activation was impaired. organism: Rattus norvegicus tissue_or_cell_type: Rat gastrocnemius receptor preparations and perfused hindquarter experimental_model: Partially purified rat gastrocnemius receptors. limitations: A depletion experiment; not isolated Mg binding to a particular receptor site. cross_nutrient: Magnesium -> insulin signaling -> carbohydrate handling. [mg-suarez1995] Impaired tyrosine-kinase activity of muscle insulin receptors from hypomagnesaemic rats (1995). https://pubmed.ncbi.nlm.nih.gov/8582534/ DOI: 10.1007/bf00401757
Complete structured claim and evidenceChromium-associated GLUT4 trafficking in this study was not accompanied by enhancement of the examined insulin-receptor, IRS-1, PI3K or Akt signaling steps.
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
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.