Component
Acacb-null mouse genotype
Acacb-null mouse genotype. Species, exposure and limitations are retained in each linked claim.
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 it acts on
Acacb-null mice had approximately 30-fold lower muscle malonyl-CoA and 10-fold lower heart malonyl-CoA than wild-type mice.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/biotin-research/11283375.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d8998a50f9e50b7528afe992760b547dcf705d04f873f0f4f11ed81e71b48249", "start_char": 0, "end_char": 894, "text_sha256": "d8998a50f9e50b7528afe992760b547dcf705d04f873f0f4f11ed81e71b48249"}
- experimental_model
- Acacb-knockout mice compared with wild type
- exposure
- Genetic deletion
- limitations
- Loss of one enzyme in mice is not dietary biotin deficiency, which can affect several enzymes; this is not evidence for inducing deficiency to change body weight.
- nutrient_topic
- Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
- organism
- Mus musculus
- plain_language
- Loss of ACC2 lowered the local metabolite that helps restrain fatty-acid entry.
- primary_references
- [b7-p11283375] Continuous fatty acid oxidation and reduced fat storage in mice lacking acetyl-CoA carboxylase 2. (2001). https://pubmed.ncbi.nlm.nih.gov/11283375/ DOI: 10.1126/science.1056843
- tissue_or_cell_type
- Heart, skeletal muscle and adipose tissue
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 715–726
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Acacb-knockout mice compared with wild type · source_derived_draft · unverified_draft
### b7-acc2-null-malonyl Acacb-null mice had approximately 30-fold lower muscle malonyl-CoA and 10-fold lower heart malonyl-CoA than wild-type mice. Condition category: machinery_impairment nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Loss of ACC2 lowered the local metabolite that helps restrain fatty-acid entry. organism: Mus musculus tissue_or_cell_type: Heart, skeletal muscle and adipose tissue experimental_model: Acacb-knockout mice compared with wild type limitations: Loss of one enzyme in mice is not dietary biotin deficiency, which can affect several enzymes; this is not evidence for inducing deficiency to change body weight. exposure: Genetic deletion evidence_span: {"source_cache": "artifacts/biotin-research/11283375.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d8998a50f9e50b7528afe992760b547dcf705d04f873f0f4f11ed81e71b48249", "start_char": 0, "end_char": 894, "text_sha256": "d8998a50f9e50b7528afe992760b547dcf705d04f873f0f4f11ed81e71b48249"} [b7-p11283375] Continuous fatty acid oxidation and reduced fat storage in mice lacking acetyl-CoA carboxylase 2. (2001). https://pubmed.ncbi.nlm.nih.gov/11283375/ DOI: 10.1126/science.1056843
Complete structured claim and evidenceSoleus fatty-acid oxidation was about 30% higher in Acacb-null mice than in wild-type mice.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/biotin-research/11283375.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d8998a50f9e50b7528afe992760b547dcf705d04f873f0f4f11ed81e71b48249", "start_char": 0, "end_char": 894, "text_sha256": "d8998a50f9e50b7528afe992760b547dcf705d04f873f0f4f11ed81e71b48249"}
- experimental_model
- Acacb-knockout mice compared with wild type
- exposure
- Genetic deletion
- limitations
- Loss of one enzyme in mice is not dietary biotin deficiency, which can affect several enzymes; this is not evidence for inducing deficiency to change body weight.
- nutrient_topic
- Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
- organism
- Mus musculus
- plain_language
- The enzyme deletion changed fuel use in mouse muscle.
- primary_references
- [b7-p11283375] Continuous fatty acid oxidation and reduced fat storage in mice lacking acetyl-CoA carboxylase 2. (2001). https://pubmed.ncbi.nlm.nih.gov/11283375/ DOI: 10.1126/science.1056843
- tissue_or_cell_type
- Heart, skeletal muscle and adipose tissue
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 728–739
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Acacb-knockout mice compared with wild type · source_derived_draft · unverified_draft
### b7-acc2-null-oxidation Soleus fatty-acid oxidation was about 30% higher in Acacb-null mice than in wild-type mice. Condition category: machinery_impairment nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The enzyme deletion changed fuel use in mouse muscle. organism: Mus musculus tissue_or_cell_type: Heart, skeletal muscle and adipose tissue experimental_model: Acacb-knockout mice compared with wild type limitations: Loss of one enzyme in mice is not dietary biotin deficiency, which can affect several enzymes; this is not evidence for inducing deficiency to change body weight. exposure: Genetic deletion evidence_span: {"source_cache": "artifacts/biotin-research/11283375.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d8998a50f9e50b7528afe992760b547dcf705d04f873f0f4f11ed81e71b48249", "start_char": 0, "end_char": 894, "text_sha256": "d8998a50f9e50b7528afe992760b547dcf705d04f873f0f4f11ed81e71b48249"} [b7-p11283375] Continuous fatty acid oxidation and reduced fat storage in mice lacking acetyl-CoA carboxylase 2. (2001). https://pubmed.ncbi.nlm.nih.gov/11283375/ DOI: 10.1126/science.1056843
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.