Exports liver fat
Hepatic triglyceride packaging into VLDL
Also searched as Hepatic triglyceride packaging into VLDL.
The balance here is a Literal Trade Between two Places — the liver and the blood. VLDL export is how the liver gets fat out of itself. Raise it and hepatic steatosis falls; the same move raises serum triglycerides, because the fat has to go somewhere. Lower it and triglycerides fall while fat accumulates in the liver. There is NO setting that wins both. Which one you would rather have depends on which is currently the problem.
In depth
The lipoprotein that packages hepatic triglyceride and ships it out of the liver — the fat-export freight line.
What drives it
Builds mitochondria reduces it.
Chen 2010, J Biol Chem 285:25996 — PGC-1α stimulates hepatic VLDL assembly and secretion through activation of CideB.
What it drives
It reduces Clears liver fat.
Hepatic VLDL-secretion study 2010 — impaired VLDL secretion (loss of microsomal triglyceride transfer protein) drives hepatic triglyceride accumulation and steatohepatitis; VLDL export protects the liver from steatosis. PMID 20392512. Human genetics settles the direction: people carrying rare variants in APOB or MTTP have VLDL secretion virtually eliminated, with a resulting increase in hepatic steatosis — and familial abetalipoproteinemia shows near-complete absence of apoB-containing lipoproteins. Export is the drain; block the drain and the liver fills. MTP is described as absolutely required for VLDL assembly. And fat blocks its own exit — A self-amplifying loop: free-fatty-acid accumulation in the liver causes chronic endoplasmic reticulum stress, ER stress increases apoB100 degradation, and losing apoB100 reduces the liver's ability to export triglyceride, worsening the steatosis that started it. Insulin does the same thing deliberately: insulin directly targets apoB100 for degradation, so hyperinsulinemia suppresses the export route. PMID 20392512
It increases Triglycerides.
Lipoprotein-metabolism review (Endotext NBK326742) — VLDL is the triglyceride-rich lipoprotein that exports hepatic triglyceride into the circulation, raising plasma triglycerides. NBK326742. VLDL is the vehicle: each particle carries one molecule of apoB-100 plus varying triacylglycerol and cholesteryl ester, and its physiological job is transporting energy from the liver to the periphery — so plasma triglyceride is largely a readout of hepatic export. Causal demonstration: adenoviral mtp overexpression raised hepatic VLDL-triglyceride secretion without changing apoB100 synthesis — more triglyceride loaded into the same number of particles, not more particles. And it only worked on an apoB100 background, and only where hepatic triglyceride or apoB100 was already elevated — the export machinery is substrate-limited, not rate-limited, under normal conditions.
Blends that modulate it
Each blend page names this pathway and carries the study behind its claim.
See it on the map
Open the causal map to follow this pathway upstream and downstream, arrow by arrow, each with its study.