ID: polydatin
Aliases: piceid, resveratrol glucoside
Type: compound
Route/form: oral supplement/food component unless otherwise specified
Status: research
Evidence level: preclinical
Best data tier: non-human experimental
Support scope: non-human/mechanistic, review/regulatory
Source types: preclinical, review
Linked sources: 3
Broad outcomes: Fat loss / metabolic health
Reading note: These are curation notes anchored to linked sources, not a clinical recommendation or protocol.
Targets / mechanism
- ACADVL
- fatty-acid oxidation
- adipocyte browning
Optimization domains
- fat loss
- metabolic health
- adipocyte browning
- natural product
Research basis
- A preclinical report identifies ACADVL as a target through which polydatin promotes adipocyte browning and fatty-acid oxidation in obesity models.
- Useful target-mechanism neighbor for other browning and mitochondrial-fat-oxidation claims.
Limits, risks, and missing evidence
- No human obesity outcome trial was identified for this specific target claim.
- Rodent browning signals often fail to become practical human fat-loss interventions.
Risk flags
- preclinical only
- translational gap
- standardization uncertainty
- limited human data
Linked papers, labels, and reviews
- Polydatin targets ACADVL to combat obesity by promoting adipocyte browning and activating fatty acid oxidation
preclinical / jove_polydatin_acadvl_2026
Diet-induced obesity mouse and adipocyte mechanism source. - Pharmacological effects of polydatin in the treatment of metabolic diseases: A review
review / sciencedirect_polydatin_metabolic_review_2022
Review of polydatin metabolic-disease pharmacology through obesity, diabetes, dyslipidemia, NAFLD, and related models. - Polydatin: a potential NAFLD therapeutic drug that regulates mitochondrial autophagy through SIRT3-FOXO3-BNIP3 and PINK1-PRKN mechanisms
preclinical / pubmed_polydatin_nafld_sirt3_2024
Related metabolic-disease source for polydatin effects on mitochondrial/autophagy pathways in NAFLD models.