Component
Human hydroxysteroid dehydrogenase 10 / HSD17B10
Context-specific entity; species, compartment and exposure are stated on each 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
HSD17B10 encodes the 2-methyl-3-hydroxybutyryl-CoA dehydrogenase step of isoleucine metabolism.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Established biochemical function in a primary loss-of-function/rescue study.
- limitations
- The protein also has essential functions beyond this reaction; metabolic activity alone does not explain its disease phenotype.
- nutrient_topic
- L-Isoleucine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Isoleucine
- plain_language
- Another enzyme changes the intermediate before the final carbon split.
- primary_references
- A non-enzymatic function of 17beta-hydroxysteroid dehydrogenase type 10 is required for mitochondrial integrity and cell survival. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20077426/ · DOI 10.1002/emmm.200900055
L-Isoleucine: transport, translation, catabolism and cross-nutrient mechanisms (2026-09-19) · lines 210–216
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Established biochemical function in a primary loss-of-function/rescue study. · source_derived_draft · unverified_draft
## isoleucine-hsd10-reaction Another enzyme changes the intermediate before the final carbon split. HSD17B10 encodes the 2-methyl-3-hydroxybutyryl-CoA dehydrogenase step of isoleucine metabolism. Model: Established biochemical function in a primary loss-of-function/rescue study. Limitations: The protein also has essential functions beyond this reaction; metabolic activity alone does not explain its disease phenotype. Evidence access: Primary abstract A non-enzymatic function of 17beta-hydroxysteroid dehydrogenase type 10 is required for mitochondrial integrity and cell survival. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20077426/ · DOI 10.1002/emmm.200900055
Complete structured claim and evidence
Where it participates (unsigned role)
Two HSD10 and four ACAT1 deficiency cases shared elevated 2-methyl-3-hydroxybutyrate/tiglylglycine patterns but had different clinical courses.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Six-patient human clinical and molecular study.
- limitations
- Small series; the suggested neurosteroid explanation was not experimentally proven by these comparisons.
- nutrient_topic
- L-Isoleucine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Isoleucine
- plain_language
- Similar metabolite readings can arise from different machinery failures.
- primary_references
- Clinical and molecular analysis of 6 Chinese patients with isoleucine metabolism defects: identification of 3 novel mutations in the HSD17B10 and ACAT1 gene. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28875337/ · DOI 10.1007/s11011-017-0097-y
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
L-Isoleucine: transport, translation, catabolism and cross-nutrient mechanisms (2026-09-19) · lines 250–256
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Six-patient human clinical and molecular study. · source_derived_draft · unverified_draft
## isoleucine-catabolic-differential Similar metabolite readings can arise from different machinery failures. Two HSD10 and four ACAT1 deficiency cases shared elevated 2-methyl-3-hydroxybutyrate/tiglylglycine patterns but had different clinical courses. Model: Six-patient human clinical and molecular study. Limitations: Small series; the suggested neurosteroid explanation was not experimentally proven by these comparisons. Evidence access: Primary abstract Clinical and molecular analysis of 6 Chinese patients with isoleucine metabolism defects: identification of 3 novel mutations in the HSD17B10 and ACAT1 gene. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28875337/ · DOI 10.1007/s11011-017-0097-y
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.