Component

Mouse sirtuin 1 / Sirt1

Context-specific entity; species, compartment and exposure are stated on each claim.

3 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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.

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.

Recorded relationships

What it acts on

  1. Adult-induced Sirt1 deletion prevented resveratrol-associated improvements in mouse skeletal-muscle mitochondrial function at both tested dietary doses.

    Mouse sirtuin 1 / Sirt1 → Resveratrol-associated mouse muscle mitochondrial improvement source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    High-fat-fed mice receiving approximately 25–30 or 215–230 mg/kg/day.
    limitations
    Adult knockout, tissue context and high-fat diet matter; not a human niacin-deficiency experiment.
    nutrient_topic
    Resveratrol collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Resveratrol
    plain_language
    A response can require intact machinery even if upstream signals still change.
    primary_references
    SIRT1 is required for AMPK activation and the beneficial effects of resveratrol on mitochondrial function. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22560220/ · DOI 10.1016/j.cmet.2012.04.003
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Resveratrol: metabolites, target selectivity and cross-nutrient mechanisms (2026-09-19) · lines 174–180

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · High-fat-fed mice receiving approximately 25–30 or 215–230 mg/kg/day. · source_derived_draft · unverified_draft

    ## resveratrol-mouse-sirt1-loss A response can require intact machinery even if upstream signals still change. Adult-induced Sirt1 deletion prevented resveratrol-associated improvements in mouse skeletal-muscle mitochondrial function at both tested dietary doses. Model: High-fat-fed mice receiving approximately 25–30 or 215–230 mg/kg/day. Limitations: Adult knockout, tissue context and high-fat diet matter; not a human niacin-deficiency experiment. Evidence access: Primary full text SIRT1 is required for AMPK activation and the beneficial effects of resveratrol on mitochondrial function. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22560220/ · DOI 10.1016/j.cmet.2012.04.003
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. In mouse C2C12 cells, 25 micromolar resveratrol activated AMPK in a Sirt1-dependent manner; at 50 micromolar, activation could occur independently of Sirt1.

    Resveratrol → Mouse AMPK complexes source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Mouse muscle-cell dose comparison.
    limitations
    Neither concentration is a demonstrated human muscle exposure.
    nutrient_topic
    Resveratrol collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Resveratrol
    plain_language
    The route to the same signaling node changes with exposure.
    primary_references
    SIRT1 is required for AMPK activation and the beneficial effects of resveratrol on mitochondrial function. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22560220/ · DOI 10.1016/j.cmet.2012.04.003

    Resveratrol: metabolites, target selectivity and cross-nutrient mechanisms (2026-09-19) · lines 182–188

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse muscle-cell dose comparison. · source_derived_draft · unverified_draft

    ## resveratrol-mouse-ampk-dose The route to the same signaling node changes with exposure. In mouse C2C12 cells, 25 micromolar resveratrol activated AMPK in a Sirt1-dependent manner; at 50 micromolar, activation could occur independently of Sirt1. Model: Mouse muscle-cell dose comparison. Limitations: Neither concentration is a demonstrated human muscle exposure. Evidence access: Primary full text SIRT1 is required for AMPK activation and the beneficial effects of resveratrol on mitochondrial function. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22560220/ · DOI 10.1016/j.cmet.2012.04.003
    Complete structured claim and evidence

  2. ACMSD inhibition increased de novo NAD synthesis and SIRT1-related mitochondrial function in the mouse experiments.

    Mouse ACMS decarboxylase / Acmsd → NAD+ source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Mouse genetic/pharmacological work within a study also using C. elegans.
    limitations
    Not a human longevity outcome or evidence for tryptophan megadoses.
    nutrient_topic
    Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
    plain_language
    Restricting one exit route increased flow toward NAD in a preclinical model.
    primary_references
    De novo NAD+ synthesis enhances mitochondrial function and improves health. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30356218/ · DOI 10.1038/s41586-018-0645-6

    Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 234–240

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse genetic/pharmacological work within a study also using C. elegans. · source_derived_draft · unverified_draft

    ## tryptophan-acmsd-inhibition-nad Restricting one exit route increased flow toward NAD in a preclinical model. ACMSD inhibition increased de novo NAD synthesis and SIRT1-related mitochondrial function in the mouse experiments. Model: Mouse genetic/pharmacological work within a study also using C. elegans. Limitations: Not a human longevity outcome or evidence for tryptophan megadoses. Evidence access: Primary abstract De novo NAD+ synthesis enhances mitochondrial function and improves health. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30356218/ · DOI 10.1038/s41586-018-0645-6
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards