Adipose tissue enzymes

It is quite possible that both of these transitions occur with the avian liver and bovine adipose tissue enzymes as well, but that both are rapid and, therefore, not readily observed. 

Very Htfle data are available regarding effects of anaboHc steroid implants on the Hpid metaboHsm in growing mminants. Lipogenic enzyme activity and fatty acid synthesis in vitro were elevated in subcutaneous adipose tissue from bulls implanted with estradiol (44), which may account for the increase in fat content of carcasses reported in some studies. TBA implants have no effect on Hpogenesis in intact heifers, and only tend to reduce Hpogenic enzyme activities in ovariectomized heifers (45). 

Endothelial anchored enzyme in muscle and adipose tissue primarily responsible for hydrolysis of chylomicron and VLDL triglycerides. 

A xenobiotic is said to be stored when it is not available to sites of metabolism or action and is not available for excretion. In other words, it is held in an inert position from a toxicological point of view, where it is not able to express toxic action or to be acted upon by enzymes. A xenobiotic is stored when it is located in a fat depot (adipose tissue), bound to an inert protein or other cellular macromolecule, or simply held in a membrane that does not have any toxicological function (i.e., it does not contain or represent a site of toxic action, neither does it contain enzymes that can degrade the xenobiotic). 

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. 

The glycerol produced by the action of hormone-sensitive lipase in the adipose tissue cannot be utilized by adipose tissue itself. Adipose cells lack the enzyme glycerol kinase, which is necessary to convert glycerol to glycerol phosphate. 

Triglyceride and fatty acid synthesis are promoted by insulin stimulation of liver and adipose tissues by causing the phosphorylation of the first and controlling enzyme in the pathway acetyl-CoA carboxylase (see Section 6.3.2). This enzyme catalyses the formation of malonyl-CoA and requires both allosteric activation by citrate and covalent modification for full activity. 

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. 

Fatty acid utilized by muscle may arise from storage triglycerides from either adipose tissue depot or from lipid stores within the muscle itself. Lipolysis of adipose triglyceride in response to hormonal stimulation liberates free fatty acids (see Section 9.6.2) which are transported through the bloodstream to the muscle bound to albumin. Because the enzymes of fatty acid oxidation are located within subcellular organelles (peroxisomes and mitochondria), there is also need for transport of the fatty acid within the muscle cell this is achieved by fatty acid binding proteins (FABPs). Finally, the fatty acid molecules must be translocated across the mitochondrial membranes into the matrix where their catabolism occurs. To achieve this transfer, the fatty acids must first be activated by formation of a coenzyme A derivative, fatty acyl CoA, in a reaction catalysed by acyl CoA synthetase. 

---