Fatty acid activation
Acyl-CoA synthetase (ACSL)
Also searched as Acyl-CoA synthetase (ACSL).
The balance here is real and both directions are load-bearing. Released fat cannot be burned or stored until this enzyme activates it — so it is the gateway to disposal, which is the thing that makes release worthwhile. But that same activated form is the inhibitor: it binds the activator the main lipase needs, blocks the second lipase, and feeds the pathway that ends release entirely. The enzyme that opens the exit also arms the TRAP. Neither more nor less is the answer; flux is.
In depth
The enzyme that converts released fat into the form that shuts release down.
What drives it
Fatty-acid oxidation increases it.
PPARalpha induces ACSL1 transcription, coupling fatty-acid influx to long-chain acyl-CoA formation. PMID 9353271
What it drives
It increases Activated fatty acids.
The enzyme that sets the trap it also needs. 'lipolysis derived FFAs need to be activated to metabolizable lc-CoAs via the long-chain acyl coenzyme A synthetase (ACSL) for further metabolization such as beta-oxidation, synthesis of complex lipids, or protein acylation' (doi 10.3389/fphys.2022.826314). ⇒ NO disposal without this step, and NO self-inhibition without it either. doi 10.3389/fphys.2022.826314
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.