Component
SELENOM
ER selenoprotein with experimental links to hypothalamic leptin signaling; physiological substrates remain unresolved.
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
SELENOM depletion reduced leptin-evoked STAT3 phosphorylation in hypothalamic-cell experiments.
Experimental context and source evidence
- cell_type
- mHypoE-44 hypothalamic cells
- experimental_model
- Knockdown and knockout
- limitations
- Does not demonstrate direct enzymatic action on STAT3.
- organism
- mouse
Selenium: literature corrections and mechanism additions · lines 786–796
Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Knockdown and knockout · secondary_verified · secondary_verified
## selenom-supports-leptin-stat3-response SELENOM helped these cells respond to leptin. SELENOM depletion reduced leptin-evoked STAT3 phosphorylation in hypothalamic-cell experiments. Organism: mouse Cell type: mHypoE-44 hypothalamic cells Experimental model: Knockdown and knockout Limitations: Does not demonstrate direct enzymatic action on STAT3. Primary reference: [Selenoprotein M Promotes Hypothalamic Leptin Signaling and Thioredoxin Antioxidant Activity](https://pmc.ncbi.nlm.nih.gov/articles/PMC8617589/)
Complete structured claim and evidenceSELENOM perturbations changed thioredoxin activity, with loss reducing the measured activity.
Experimental context and source evidence
- cell_type
- hypothalamic cells
- experimental_model
- Loss and expression experiments
- limitations
- The direct SELENOM substrate was not established.
- organism
- mouse
Selenium: literature corrections and mechanism additions · lines 798–808
Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Loss and expression experiments · secondary_verified · secondary_verified
## selenom-supports-thioredoxin-activity SELENOM supported a cellular thioredoxin activity readout. SELENOM perturbations changed thioredoxin activity, with loss reducing the measured activity. Organism: mouse Cell type: hypothalamic cells Experimental model: Loss and expression experiments Limitations: The direct SELENOM substrate was not established. Primary reference: [Selenoprotein M Promotes Hypothalamic Leptin Signaling and Thioredoxin Antioxidant Activity](https://pmc.ncbi.nlm.nih.gov/articles/PMC8617589/)
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.