Fat transport protein
The balance here is real and both directions matter. These proteins buffer free fatty acids inside the cell, and that buffering is one of the three named determinants of how much released fat gets put straight back into storage. But they are also the delivery system: the same carrier ferries released fat between tissues and into the nucleus, where it is required for the signaling that keeps the fat cell working properly at all. Remove the sponge and you lose the courier.
In depth
Proteins that mop up released fatty acids inside the cell before they can leave.
What drives it
Releases stored fat increases it.
The sponge is also the courier, and both directions are on the record. 'lipolysis-derived fatty acids are shuttled by fatty acid-binding proteins (FABPs) to the nucleus, where they are necessary for proper PPAR signaling' (doi 10.3389/fphys.2022.826314). And systemically: 'The circulating lipid chaperone called A-FABP has been reported to facilitate ffa import from wat into bat.' ⇒ removing it would cost the delivery system as well as the buffer. A structural confirmation of the dual role: HSL's 'N-terminal domain binds the fatty acid binding protein 4 (FABP4), and participates in HSL dimer formation' (Cell Metab, 'Nuclear hormone-sensitive lipase regulates adipose tissue mass and adipocyte metabolism'). The buffer protein is physically bound to the lipase itself. doi 10.3389/fphys.2022.826314
What it drives
It increases Fat re-storage.
'It is believed that the primary factors determining the extent of reesterification within the adipocyte is the intracellular FFAs buffering via FABPs, the ability of plasma to carry away released FFA, and the availability of glucose' (doi 10.3389/fphys.2022.826314) — one of the three named determinants. 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.