The Lactate Veto
You want this loop understood rather than fought. Insulin does not only erase the signal directly; it also makes the fat cell release lactate, which binds back onto this receptor and inhibits the making of the messenger. It is one of a family of such vetoes: succinate, short-chain fatty acids, medium and long chain fatty acids, ketone bodies, nicotinic acid and a neuropeptide all have their own receptors doing the same job. That list includes things people take deliberately.
In depth
A receptor on the fat cell for lactate — which the cell releases itself, on insulin's instruction, to shut its own release down.
What drives it
Insulin sensitivity increases it.
'an AUTOCRINE lactate loop mediates insulin-dependent inhibition of lipolysis through GPR81' (doi 10.3389/fphys.2022.826314, citing Ahmed et al. 2010). And the whole family is named: 'succinate, short-chain fatty acids, medium- and long-chain fatty acids, ketone body beta-hydroxybutyrate, nicotinic acid and neuropeptide Y can also conduct anti-lipolytic effects via... GPR91, GPR43, GPR120, GPR109A and Y1R.' that list includes things taken deliberately as supplements. doi 10.3389/fphys.2022.826314
What it drives
It reduces The cell's go-signal.
'the mechanism underlying the insulin-induced reduction in adipocyte cAMP levels is more complex and involves insulin-stimulated release of lactate from adipocytes to inhibit cAMP formation via GPR81. Gi-coupled receptor GPR81 is specially expressed in adipocytes and serves as a lactate receptor'. doi 10.3389/fphys.2022.826314
See it on the map
Open the causal map to follow this pathway upstream and downstream, arrow by arrow, each with its study.