Molecular target
PPAR-γ
Nuclear receptor regulating adipocyte differentiation and insulin sensitivity. Targeted by thiazolidinediones (pioglitazone) and modulated by several plant compounds (genistein, curcumin, resveratrol).
Educational use only. This page summarizes published research and traditional-use records for educational purposes. It does not diagnose, treat, cure, or prevent any disease. Do not start, stop, or change medications based on this information. Discuss any decisions about therapies — pharmaceutical or botanical — with a qualified clinician who knows your medical history.
No PHI / HIPAA notice: Do not share Protected Health Information (PHI) of any patient on this site — including names, dates of birth, addresses, MRNs, or any identifying information. Use abstract case framing only. Sharing PHI with non-covered entities risks HIPAA violation regardless of platform capability.
Pharmaceutical agents
Drugs that act on PPAR-γ
These medications have PPAR-γ among their molecular targets. Sharing a target is a mechanistic relationship — it does not make any plant below an alternative to, or substitute for, these drugs.
Botanical connections
Plants whose compounds act on PPAR-γ
Each plant below contains a named compound documented to act on PPAR-γ. The compound and the reason for the connection are shown on every edge — a shared mechanism, not a therapeutic equivalence.
- FalcarindiolPolyacetylene (polyyne)
Reported in vitro to inhibit 5-lipoxygenase and cyclooxygenase (Zschocke et al., 1997); additionally reported to activate Nrf2/ARE pathway, inducing antioxidant and phase-2 drug-metabolizing enzymes in cultured hepatic cells (Ohnuma et al., 2009); also demonstrated partial PPARγ agonism in reporter assays (Atanasov et al., 2013).
- Notoethers A–H; Notoincisols A–CPolyyne hybrid compounds
Novel polyacetylene derivatives isolated from roots and rhizomes; several demonstrated PPARγ activation in luciferase reporter assays (HEK-293 cells) in vitro (Liu et al., 2014).
- α-Linolenic acid (ALA)Omega-3 fatty acid
Seed oil is rich in ALA; omega-3 fatty acids are broadly investigated for modulation of inflammatory pathways including NF-κB and PPAR-γ activation.
- Palmitoleic acidMonounsaturated fatty acid (ω-7)
Pulp oil contains high levels of palmitoleic acid; investigated in the context of skin barrier function and lipid metabolism, potentially via PPAR-γ pathways.
- Berberineisoquinoline alkaloid
Activates AMPK (insulin-sensitizing, lipid-lowering), provides modest DPP-4 inhibition, modulates gut microbiota, and inhibits intestinal disaccharidases — collectively the basis for its glucose-lowering effect.
- EmbelinNaphthoquinone (benzoquinone derivative)
Embelin is the principal bioactive constituent. Preclinical studies report it may activate AMPK and PPAR-γ pathways relevant to glucose and lipid homeostasis, sensitise insulin receptor signalling, modulate NF-κB and TNF-α inflammatory pathways, inhibit HMG-CoA reductase contributing to observed lipid-lowering effects, and interact with oestrogen receptors (postulated basis for reported reproductive/contraceptive effects). All mechanistic data are predominantly in vitro or animal-derived.
- Procyanidin type Aflavonoid (polymer)
Modulates PPAR-γ signaling, contributing to insulin sensitization in adipose tissue.
- GenisteinIsoflavone
Beyond estrogen-receptor binding, genistein is a classically characterized protein-tyrosine-kinase inhibitor and has been studied for anti-angiogenic (VEGF) activity in preclinical cancer models. Research only — not a treatment claim.
- PMI-5011 polyphenol complex (incl. DMC-2)Polyphenol / dihydrochalcone
In vitro and animal studies report that the PMI-5011 ethanolic extract and its constituent DMC-2 may improve insulin sensitivity via AMPK activation and PPAR-γ modulation; mechanisms were investigated in C57BL/6 mouse models and corroborated in a small human RCT.
- Trans-resveratrolStilbenoid polyphenol
Alongside SIRT1/NF-kB activity, resveratrol has been studied for PI3K–Akt–mTOR pathway modulation and anti-angiogenic (VEGF) effects in preclinical models. Research only — not a treatment claim.