Diacylglycerol signaling
This route genuinely releases fat. The compounds that open it strongly are the same ones used in laboratories to promote tumors, and the opening and the harm are one act, not two.
In depth
The pocket on the conventional kinases that both the natural short-lived messenger and the tumor-promoting plant compounds fit into.
What drives it
Lipid phosphatase increases it.
Lipin-1 dephosphorylates phosphatidate to diacylglycerol, the physiological activator of conventional PKC. PMID 26658689
Fat-releasing enzyme (ATGL) modulates it.
ATGL hydrolyzes triacylglycerol to diacylglycerol, a second source of the conventional-PKC activator. Sources: doi 10.1186/s12944-020-01286-8; PMC8829450; PMID 23066022. doi 10.1186/s12944-020-01286-8 · PMID 23066022 · PMC8829450
What it drives
It increases Releases stored fat.
A route that works and is still refused. Fat release can be driven through the conventional kinases: 'One of these pathways involves PKC and can be stimulated by the phorbol ester PMA.' Those kinases are switched on at a pocket called the C1 domain, which normally receives a short-lived natural messenger. Certain plant compounds occupy that same pocket and do not wash out. A correction that matters more than the route itself: the most irritant of those plants does not actually release fat this way. When its fruit and oil were tested directly on fat cells, 'pretreatment with H89, which is a protein kinase A inhibitor, significantly abolished the... induced glycerol release', and the authors conclude it 'stimulate[S] lipolysis through HSL phosphorylation at Ser563 by PKA activation' (doi 10.1155/2014/780385 (pmc4244682) — Crotonis Fructus and Its Constituent, Croton Oil, Stimulate Lipolysis in OP9 Adipocytes). ⇒ it releases fat through the ordinary epinephrine kinase, not through this one. And the size of the effect is worth stating: 'the increase in glycerol release... Is more potent than isoproterenol' — stronger than the reference epinephrine-like agent used as the positive control. It is activation, not manufacture: 'an increase of phosphorylated hormone sensitive lipase but not nonphosphorylated HSL protein and mRNA.' the practical point: an ordinary, safe route already reaches that same kinase, so nothing is gained by taking the dangerous one. doi 10.1155/2014/780385
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.