Fig. 8.
Working model summarizing the lipolytic effect of Sct. Sct binds SctR on the plasma membrane of adipocytes to activate the cAMP-dependent PKA. PKA then phosphorylates HSL at 660ser leading to translocation of HSL from the cytosol to the phospholipid monolayer of the lipid droplet. The translocated HSL is responsible for the hydrolysis of stored triacylglycerol to release glycerol and FFAs. Norepinephrine (a catecholamine) and glucagon both activate the PKA pathway similar to Sct. TNF-α and glucocorticoids stimulate lipolysis by downregulating perilipin and enhancing the expression of ATGL, respectively. Insulin inhibits lipolysis by reducing the cAMP level through activation of PDE via the PI3K/Akt pathway. AMPK, AMP-activated protein kinase.