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Lipolysis /lᵻˈpɒlᵻsɪs/ is the breakdown of lipids and involves hydrolysis of triglycerides into glycerol and free fatty acids. The following hormones induce lipolysis[citation needed]: glucagon, epinephrine, norepinephrine, ghrelin, growth hormone, testosterone, and cortisol. 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.
Illustration of the process of lipolysis (in a fat cell) induced by high epinephrine and low insulin levels in the blood. Epinephrine binds to a beta-adrenergic receptor in the cell wall of the adipocyte, which causes cAMP to be generated inside the cell.
The cAMP activates a protein kinase, which phosphorylates and thus, in turn, activates a hormone-sensitive lipase in the fat cell.
This lipase cleaves free fatty acids from their attachment to glycerol in the fat stored in the fat droplet of the adipocyte.
The free fatty acids and glycerol are then released into the blood.
Monoglycerides are hydrolyzed by monoglyceride lipase.[1]The activity of hormone sensitive lipase is regulated by the circulation hormones insulin, glucagon, norepinephrine, and epinephrine, as shown in the diagram.
Triglycerides are transported through the blood to appropriate tissues (adipose, muscle, etc.) by lipoproteins such as Very-Low-Density-Lipoproteins (VLDL). Triglycerides present on the VLDL 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.[2] 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.[3] 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.[4]
Currently there are four main non-invasive body contouring techniques growing in the aesthetic medicine for reducing localized subcutaneous adipose tissue: low-level laser therapy (LLLT), cryolipolysis, radio frequency (RF) and high-intensity focused ultrasound (HIFU).[5][6]
Insulin action in the mediobasal hypothalamus has been shown to suppress lipolysis due to lower sympathetic nervous outflow to white adipose tissue.[7] The regulation of this process involves interactions between insulin receptors and gangliosides present in the neuronal cell membrane.[8]
Glycerol is a precursor for synthesis of triacylglycerols and of phospholipids in the liver and adipose tissue. When the body uses stored fat as a source of energy, glycerol and fatty acids are released into the bloodstream. Circulating glycerol does not glycate proteins as do glucose or fructose, and does not lead to the formation of advanced glycation endproducts (AGEs). In some[which?] organisms, the glycerol component can enter the glycolysis pathway directly and, thus, provide energy for cellular metabolism (or, potentially, be converted to glucose through gluconeogenesis).
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