In adipocytes, the succinate-activated GPR91 signaling cascade inhibits lipolysis. These metabolic processes are known as glycogenolysis, glycolysis and lipolysis. Glucagon also regulates the rate of glucose production through lipolysis. Perilipin 1A is a key protein regulator of lipolysis in adipose tissue. Please note however that lipolysis releases glycerol which can enter the pathway of gluconeogenesis. At this time, there is an up-regulation of glycogenolysis, gluconeogenesis, lipolysis, and ketogenesis. Triglycerides are broken down to fatty acids via lipolysis. The resulting insulin induced reduction in cAMP levels decreases the lipolysis rate. The remaining glucose production comes from protein breakdown, muscle glycogen, and glycerol from lipolysis. Removal of these lipid droplet coat proteins by CMA precedes lipolysis and lipophagy. Smoking also decreases weight by overexpressing the gene AZGP1 which stimulates lipolysis. One is removal by injecting compounds that trigger lipolysis, such as steroids or phosphatidylcholine. It was also reported to perform lipid-mobilizing functions such as lipolysis and steroidogenesis. The breakdown of this fat is known as lipolysis. PKA can phosphorylate lipases, perilipin 1A, and CGI-58 to increase the rate of lipolysis.