Component
Protein kinase C family
Independent biological entity. Read linked claims for experimental scope and context.
3 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 it acts on
PKC activators reduced biotin uptake in NCM460 cells; PKC inhibitors modestly increased uptake.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/biotin-research/9814986.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7cc679e31b95ae919c15fadf0d56933d2ed8074664e11cd80a96e910181857be", "start_char": 0, "end_char": 1676, "text_sha256": "7cc679e31b95ae919c15fadf0d56933d2ed8074664e11cd80a96e910181857be"}
- experimental_model
- Transport and inhibitor experiments in human NCM460 colonic epithelial cells
- exposure
- Radiolabeled biotin with sodium replacement, pantothenate and kinase modulators
- limitations
- Cell-line kinetics do not quantify microbiome contributions or demonstrate competition at ordinary dietary intakes.
- nutrient_topic
- Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
- organism
- Homo sapiens
- plain_language
- Cell signaling changes how quickly colon cells admit biotin.
- primary_references
- [b7-p9814986] Biotin uptake by human colonic epithelial NCM460 cells: a carrier-mediated process shared with pantothenic acid. (1998). https://pubmed.ncbi.nlm.nih.gov/9814986/ DOI: 10.1152/ajpcell.1998.275.5.c1365
- tissue_or_cell_type
- Colonic epithelium; NCM460 culture
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 208–219
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transport and inhibitor experiments in human NCM460 colonic epithelial cells · source_derived_draft · unverified_draft
### b7-colon-pkc PKC activators reduced biotin uptake in NCM460 cells; PKC inhibitors modestly increased uptake. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Cell signaling changes how quickly colon cells admit biotin. organism: Homo sapiens tissue_or_cell_type: Colonic epithelium; NCM460 culture experimental_model: Transport and inhibitor experiments in human NCM460 colonic epithelial cells limitations: Cell-line kinetics do not quantify microbiome contributions or demonstrate competition at ordinary dietary intakes. exposure: Radiolabeled biotin with sodium replacement, pantothenate and kinase modulators evidence_span: {"source_cache": "artifacts/biotin-research/9814986.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7cc679e31b95ae919c15fadf0d56933d2ed8074664e11cd80a96e910181857be", "start_char": 0, "end_char": 1676, "text_sha256": "7cc679e31b95ae919c15fadf0d56933d2ed8074664e11cd80a96e910181857be"} [b7-p9814986] Biotin uptake by human colonic epithelial NCM460 cells: a carrier-mediated process shared with pantothenic acid. (1998). https://pubmed.ncbi.nlm.nih.gov/9814986/ DOI: 10.1152/ajpcell.1998.275.5.c1365
Complete structured claim and evidence
What acts on it
Benfotiamine inhibited hyperglycemia-associated DAG-PKC pathway activation in the tested models.
Experimental context and source evidence
- experimental_model
- High-glucose bovine endothelial cells and diabetic rat retinal experiments.
- exposure
- Pharmacological benfotiamine in high-glucose bovine endothelial cells and diabetic rat retina; not ordinary dietary thiamine.
- limitations
- Pharmacological derivative in bovine endothelial cells/diabetic rats; not proof of human dietary-thiamine benefit or direct NADPH production by transketolase.
- nutrient_topic
- Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
- organism
- Bos taurus; Rattus norvegicus
- plain_language
- Sugar processing was linked to a lipid-signaling pathway response.
- primary_references
- [b1-hammes2003] Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy (2003). https://pubmed.ncbi.nlm.nih.gov/12592403/ DOI: 10.1038/nm834
- tissue_or_cell_type
- Endothelial cultures and retina
Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1915–1925
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · High-glucose bovine endothelial cells and diabetic rat retinal experiments. · source_derived_draft · unverified_draft
### b1-benfotiamine-pkc Benfotiamine inhibited hyperglycemia-associated DAG-PKC pathway activation in the tested models. Condition category: normal nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Sugar processing was linked to a lipid-signaling pathway response. organism: Bos taurus; Rattus norvegicus tissue_or_cell_type: Endothelial cultures and retina experimental_model: High-glucose bovine endothelial cells and diabetic rat retinal experiments. limitations: Pharmacological derivative in bovine endothelial cells/diabetic rats; not proof of human dietary-thiamine benefit or direct NADPH production by transketolase. exposure: Pharmacological benfotiamine in high-glucose bovine endothelial cells and diabetic rat retina; not ordinary dietary thiamine. [b1-hammes2003] Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy (2003). https://pubmed.ncbi.nlm.nih.gov/12592403/ DOI: 10.1038/nm834
Complete structured claim and evidence
Where it participates (unsigned role)
Berberine increased INSR mRNA and protein in human liver cells through PKC-dependent promoter activation.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/berberine-research/19059538.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "70e22b36b13efcbb36d7f27b417fe72dc96ba2f384f01a8d037bfc2d3213ef23", "start_char": 0, "end_char": 1461, "text_sha256": "70e22b36b13efcbb36d7f27b417fe72dc96ba2f384f01a8d037bfc2d3213ef23"}
- experimental_model
- Promoter assays, gene silencing and insulin-dependence experiments
- exposure
- Berberine with or without insulin, INSR siRNA or PKC inhibition
- limitations
- This insulin-dependent route does not replace insulin in insulin-deficient disease. Other models show insulin-independent routes; those observations are not discarded.
- nutrient_topic
- Berberine research collection; topical membership is not evidence of a direct dietary effect. · Berberine
- organism
- Human liver cells and separate rodent experiments
- plain_language
- The cells increased the machinery that receives an insulin signal.
- primary_references
- [berberine-p19059538] Berberine reduces insulin resistance through protein kinase C-dependent up-regulation of insulin receptor expression. (2009). https://pubmed.ncbi.nlm.nih.gov/19059538/ DOI: 10.1016/j.metabol.2008.08.013
- tissue_or_cell_type
- Insulin receptor expression and glucose consumption
Berberine: metabolism, nutrient connections and drug interactions (2026-09-17) · lines 493–504
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Promoter assays, gene silencing and insulin-dependence experiments · source_derived_draft · unverified_draft
### berberine-insr-expression Berberine increased INSR mRNA and protein in human liver cells through PKC-dependent promoter activation. Condition category: normal nutrient_topic: Berberine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The cells increased the machinery that receives an insulin signal. organism: Human liver cells and separate rodent experiments tissue_or_cell_type: Insulin receptor expression and glucose consumption experimental_model: Promoter assays, gene silencing and insulin-dependence experiments limitations: This insulin-dependent route does not replace insulin in insulin-deficient disease. Other models show insulin-independent routes; those observations are not discarded. exposure: Berberine with or without insulin, INSR siRNA or PKC inhibition evidence_span: {"source_cache": "artifacts/berberine-research/19059538.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "70e22b36b13efcbb36d7f27b417fe72dc96ba2f384f01a8d037bfc2d3213ef23", "start_char": 0, "end_char": 1461, "text_sha256": "70e22b36b13efcbb36d7f27b417fe72dc96ba2f384f01a8d037bfc2d3213ef23"} [berberine-p19059538] Berberine reduces insulin resistance through protein kinase C-dependent up-regulation of insulin receptor expression. (2009). https://pubmed.ncbi.nlm.nih.gov/19059538/ DOI: 10.1016/j.metabol.2008.08.013
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.