Adipose triglyceride lipase

Miyoshi, H., Perfield, J.W., II, Souza, S.C., Shen, W.J., Zhang, H.H., et al. 2007. Control of adipose triglyceride lipase action by serine 517 of perilipin A globally regulates protein kinase A-stimulated lipolysis in adipocytes. J. Biol. Chem. 282 996-1002. 

Bakke SS, Moro C, Nikolic N, et al. Palmitic acid follows a different metabolic pathway than oleic acid in human skeletal muscle cells lower lipolysis rate despite an increased level of adipose triglyceride lipase. Biochim Biophys Acta. 2012, 1821(10) l323-33. 

Adipose tissue triglyceride lipase Triglyceride free fatty acids + glycerol phosphorylated... 

There are two types of cell membrane receptor (a and jS) for adrenaline. -Receptors which are inhibited by -blockers such as propanolol are the main type of receptor in muscle, heart, adipose tissue and many other tissues. They interact with and activate adenylate cyclase in the cell membrane so that the effect of adrenaline on muscle or adipose tissue is to increase the concentration of cAMP in the cell and thus to activate protein kinase. Stimulation of glycogen breakdown by adrenaline in muscle is then mediated by a cascade mechanism similar to that involved in the stimulation of glycogenolysis in liver by glucagon (page 353). Breakdown of triglycerides in adipose tissue, as in liver, occurs as a result of activation of triglyceride lipase by phosphorylation. 

The immediate sources of energy for the body are the free fatty acids in the circulation liberated from adipose triglycerides by the enzyme lipase. These free fatty acids are oxidized or burned by a systematic process called betaoxidation, whereby 2-carbon fragments are successively cleaved from the fatty acid molecule to form acetyl CoA which releases energy upon completing the Krebs cycle (TG cycle). 

Figure 3. Adipose tissue triglyceride lipase. + denotes activation.

Intravenous lipid emulsion particles are hydrolyzed in the bloodstream by the enzyme lipoprotein lipase to release free fatty acids and glycerol. Free fatty acids then are be taken up into adipose tissue for storage (triglycerides), oxidized to energy in various tissues (e.g., skeletal muscle), or recycled in the liver to make lipoproteins. 

Adipose Adipose tissue is the primary storage facility for fat. Fat is stored in these tissues as an intracellular droplet of insoluble triglyceride. A hormone-sensitive lipase mobilizes triglyceride stores by hydrolysis to free fatty acids. 

The regulation of fat metabolism is relatively simple. During fasting, the rising glucagon levels inactivate fatty acid synthesis at the level of acetyl-CoA carboxylase and induce the lipolysis of triglycerides in the adipose tissue by stimulation of a hormone-sensitive lipase. This hormone-sensitive lipase is activated by glucagon and epinephrine (via a cAMP mechanism). This releases fatty acids into the blood. These are transported to the various tissues, where they are used. 

In adipose tissue, insulin stimulation suppresses triglyceride hydrolysis (to free fatty acids and glycerol) by activating cAMP phosphodiesterase (cAMP PDE). Cyclic AMP, (3, 5 cAMP), is required to stimulate hormone sensitive lipase (HSL), the enzyme which hydrolyses triglyceride within adipocytes PDE converts active 3, 5 cAMP to inactive 5 AMP thus preventing the stimulation of HSL. The net effect of insulin on lipid metabolism is to promote storage. 

High-density lipoproteins (HDL) and very low-density lipoproteins (VLDL) are synthesized in the liver. LDL is produced in the blood stream as VLDL particles are partially delipidated by lipoprotein lipase, a triglyceride hydrolysing enzyme located on the luminal surface of vessels in sites such adipose tissue. 

Lipoprotein lipase (LPL) Local enzymatic Endothelial cells within adipose tissue Lipoprotein-triglyceride hydrolysis... 

In capillaries of adipose tissue (and muscle), apoC-II activates lipoprotein lipase, the fetty adds released enter the tissue for storage, and the glycerol is retrieved by the liver, which has glycerol kinase. The chylomicron remnant is picked up by hepatocytes through the apoE receptor thus, dietary cholesterol, as well as any remaining triglyceride, is released in the hepatocyte. 

The metabolism of VLDL is very similar to that of chylomicrons, the major difference being that VLDL are assembled in hepatocytes to transport triglyceride containing fatty acids newly synthesized from excess glucose, or retrieved from the chylomicron remnants, to adipose tissue and musde. ApoB-100 is added in the hepatocytes to mediate release into the blood. Like chylomicrons, VLDL acquire apoC-II and apoE from HDL in the blood, and are metabolized by lipoprotein lipase in adipose tissue and musde. 

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