Lipolysis ( /lɨˈpɒlɨsɪs/) is the breakdown of lipids and involves the hydrolysis of triglycerides into free fatty acids followed by further degradation into acetyl units by beta oxidation. The process produces Ketones, which are found in large quantities in ketosis, a metabolic state that occurs when the liver converts fat into fatty acids and ketone bodies, which can be used by the body for energy. Lipolysis testing strips such as Ketostix are used to recognize ketosis.
The following hormones induce lipolysis: epinephrine, norepinephrine, glucagon, growth hormone, testosterone, and cortisol (although cortisol's actions are still unclear). These trigger 7TM receptors (G protein-coupled receptors), which activate adenylate cyclase. This results in increased production of cAMP, which activates protein kinase A, which subsequently activates lipases found in adipose tissue.
Triglycerides are transported through the blood to appropriate tissues (adipose, muscle, etc.) by lipoproteins such as chylomicrons. Triglycerides present on the chylomicrons undergo lipolysis by the cellular lipases of target tissues, which yields glycerol and free fatty acids. Free fatty acids released into the blood are then available for cellular uptake. Free fatty acids not immediately taken up by cells may bind to albumin for transport to surrounding tissues that require energy. Serum albumin is the major carrier of free fatty acids in the blood. The glycerol also enters the bloodstream and is absorbed by the liver or kidney where it is converted to glycerol 3-phosphate by the enzyme glycerol kinase. Hepatic glycerol 3-phosphate is converted mostly into dihydroxyacetonephosphate (DHAP) and then glyceraldehyde 3-phosphate (GA3P) to rejoin the glycolysis and gluconeogenesis pathway.
While lipolysis is triglyceride hydrolysis (the process by which triglycerides are broken down), esterification is the process by which triglycerides are formed. Esterification and lipolysis are, in essence, reversals of one another.
Lipolysis during stress occurs in the fat cells, which, in turn, increases cholestrol during chronic enduring stress.