Component
LEP
Hormonal signal acting on hypothalamic pathways involved in energy balance.
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
HFCS and sucrose produced similar 24-hour circulating leptin profiles in the crossover study.
Experimental context and source evidence
- dose
- HFCS or sucrose beverages with 3 isocaloric meals; exact sugar allocation not recovered from primary abstract
- duration
- 24-hour profiles
- evidence_access
- Primary abstract/metadata; unrecovered methods explicitly retained.
- evidence_scope
- literature_reviewed; source-specific curation
- experimental_model
- 34 adults in crossover meal study; 8 men also received pure monosaccharides
- exposure_scope
- Direct HFCS versus sucrose
- limitations
- Short feeding study; eight-man fructose/glucose comparison is a subset and does not establish long-term equivalence or appetite control.
- nutrient_topic
- HFCS chapter: actual formulation studies, component biochemistry and interventions are explicitly distinguished. · High-Fructose Corn Syrup / HFCS
- organism
- 34 adults in crossover meal study; 8 men also received pure monosaccharides
- plain_language
- HFCS and sucrose produced similar 24-hour circulating leptin profiles in the crossover study.
- primary_references
- Twenty-four-hour endocrine and metabolic profiles following consumption of high-fructose corn syrup-, sucrose-, fructose-, and glucose-sweetened beverages with meals. (2008). https://pubmed.ncbi.nlm.nih.gov/18469239/ DOI: 10.1093/ajcn/87.5.1194
- route
- Oral beverages with meals
- tissue
- 24-hour endocrine and triglyceride profiles
High-Fructose Corn Syrup: mechanism of action and metabolic impact (2026-09-20) · lines 365–375
Original AI-assisted curation of twenty primary studies and official FDA composition information, with one reused canonical glucose-transport claim. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · 34 adults in crossover meal study; 8 men also received pure monosaccharides · source_derived_draft · unverified_draft
## hfcs-acute-leptin HFCS and sucrose produced similar 24-hour circulating leptin profiles in the crossover study. Model/species: 34 adults in crossover meal study; 8 men also received pure monosaccharides Tissue: 24-hour endocrine and triglyceride profiles Exposure: HFCS or sucrose beverages with 3 isocaloric meals; exact sugar allocation not recovered from primary abstract Route: Oral beverages with meals Duration: 24-hour profiles Exposure scope: Direct HFCS versus sucrose Limits: Short feeding study; eight-man fructose/glucose comparison is a subset and does not establish long-term equivalence or appetite control. Reference: Twenty-four-hour endocrine and metabolic profiles following consumption of high-fructose corn syrup-, sucrose-, fructose-, and glucose-sweetened beverages with meals. (2008). https://pubmed.ncbi.nlm.nih.gov/18469239/ DOI: 10.1093/ajcn/87.5.1194 Access: Primary abstract/metadata; unrecovered methods explicitly retained.
Complete structured claim and evidence
Where it participates (unsigned role)
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 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.