The Door The Fat Comes In Through
You want it quiet. Shutting the door is a different strategy from burning what is already inside, and the two are not interchangeable.
In depth
A transport protein on the liver cell that pulls circulating fatty acids inside. Fat in the liver has only four possible sources: what comes in through doors like this one, what the cell builds itself, minus what it burns and what it ships out. This is the first of the four.
What drives it
Allergic signaling increases it.
Type 2 inflammation raises FATP2 in the airway lining. Verbatim: 'Inhibition of IL-4/IL-13 signaling by dupilumab reduces expression of lipid peroxidation-associated genes, including SLC27A2' (Exp Mol Med 2025, doi 10.1038/s12276-025-01440-1, PMID 40195539). human nasal epithelium; not tested in liver or fat. doi 10.1038/s12276-025-01440-1 · PMID 40195539
What it drives
It increases Clears liver fat.
10.26508/lsa.202302458 — The strictest counterfactual here, and it is a gain-of-function rescue rather than a blockade. PMID 36115008 (j Nat Med): andrographolide 'consistently reduced the expression of FATP2 in both the oleic acid-treated LO2 cells and liver tissues of HFD-fed mice... Overexpression of FATP2 abolished the lipid-lowering effect of ANDRO... Andro treatment also reduced the fatty acid uptake, which was blunted by FATP2 overexpression.' Forcing the transporter back up cancels the benefit, on two separate readouts. Independently confirmed as a real and central target by a mechanism review from another country: PMID 29936596 / doi 10.1007/s00018-018-2860-6 (Cell Mol Life Sci, University of Copenhagen) — 'CD36, FATP2 and -5 mediates increased uptake of circulating lipids in NAFLD.' Mouse and cell-line evidence only. NO human trial targets FATP2. The node exists because the formula carries a driver with a rescue-proven action on it, not because a person has been treated through it. doi 10.26508/lsa.202302458 · PMID 36115008
It increases Triglycerides.
The uptake arm of the four-pathway balance, stated by two independent reviews. Copenhagen (PMID 29936596): 'hepatic steatosis is a consequence of lipid acquisitION exceeding lipid disposal, i.e., the uptake of fatty acids and DE novo lipogenesis surpassing fatty acid oxidation and export.' Corroborated by PMID 28428362: 'Hepatic lipid accumulation may be induced by 4 separate mechanisms: (1) increased hepatic uptake of circulating fatty acids, (2) increased DE novo fatty acid synthesis, (3) decreased beta-oxidation and (4) decreased hepatic lipid export.' all four arms are now represented here: uptake (cd36, fatp2), de novo lipogenesis (lipogenesis, srebp), oxidation (fatty-acid β-oxidation, ppara), and export (vldl). Lipid export is fully represented here — `vldl` exists with an inhibitory edge into steatosis. No ingredient in the formulas is graded on VLDL export. PMID 29936596
See it on the map
Open the causal map to follow this pathway upstream and downstream, arrow by arrow, each with its study.