Limits fat uptake
CD36 fatty-acid translocase↓
Also searched as CD36 fatty-acid translocase.
You want it restrained: dialing down CD36 slows the fatty-acid influx that seeds a fatty liver.
In depth
The membrane transporter that pulls circulating fatty acids into the liver — the inflow valve that, wide open, floods hepatocytes with fat.
What drives it
Blocks new fat cells increases it.
Zhou 2008, Gastroenterology 134:556 — the hepatic fatty-acid transporter CD36 is a transcriptional target of PPARγ (with LXR and PXR), upregulated to promote steatosis. PMID 18242221
What it drives
It increases Clears liver fat.
10.2337/db07-0907 — Koonen 2007, Diabetes 56:2863 — increased hepatic CD36 raises fatty-acid uptake and triglyceride accumulation, contributing to diet-induced hepatic steatosis. The quantitative fact that reframes liver fat, and it argues against the popular story: in the liver, fatty acids derived from uptake of plasma free fatty acids released from adipose tissue account for approximately 70 to 80 percent of hepatic triglyceride synthesis. De-novo lipogenesis and the breakdown of remnant particles make up the remainder. Fatty acids from extrahepatic sources are stated to contribute substantially to hepatic steatosis. Implication: an intervention aimed only at de-novo lipogenesis is addressing the smaller share; the dominant inflow is fatty-acid delivery from adipose tissue, which is why adipose insulin resistance and weight sit upstream of liver fat. CD36 is one of several named uptake proteins (with SLC27A1 and FABP4) and is a PPAR target — this edge is the transport step, not the whole inflow. doi 10.2337/db07-0907
It increases Arterial plaque.
Infiltrated monocytes differentiate into macrophages, which together with vascular smooth muscle cells uptake OX-LDL via scavenger receptors such as CD36 and SR-A1. This leads to the formation of foam cells and expansion of the lipid necrotic core. Scavenger receptors ARE unregulated by cholesterol load, unlike the LDL receptor — which is why the macrophage does not stop eating, and why the foam cell forms at all. PMC5666716
It reduces Lowers cholesterol.
32958780 — insulin, fasting insulin, type 2 diabetes and blood lipids share one literature: heart, kidney, liver, and metabolic diseases share interlinked pathological mechanisms, including inflammation, oxidative stress, insulin resistance, and endothelial health issues. These four overlap by nature: fasting insulin is the level, insulin is the signaling, type 2 diabetes is the diagnosis and blood lipids are the substrate. The same driver legitimately reaches all four, and a reader should not mistake four arrows for four independent findings. doi 10.1038/s41581-026-01066-0 · PMC11725408
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.