Lipoprotein lipase triacylglycerol, adipose tissue

The action of an enzyme lipoprotein lipase in adipose tissue depletes chylomicrons and VLDLs of their triacylglycerol. The enzyme is activated by apolipoprotein C, with which it specifically interacts on the surface of chylomicrons and VLDLs. 

Triacylglycerols, either in the form of chylomicrons that are released by entero-cytes into the lymphatic system or in the form of VLDL, are hydrolyzed to fatty acids by lipoprotein lipase at the luminal side of endothelial cells lining the microvasculature of muscle and adipose tissue. Inside the cell, fatty acids are used for synthesis of triacylglycerol (adipose tissue, muscle) or oxidized to generate ATP. 

Figure 25-7. Metabolism of adipose tissue. Hormone-sensitive lipase is activated by ACTH, TSH, glucagon, epinephrine, norepinephrine, and vasopressin and inhibited by insulin, prostaglandin E, and nicotinic acid. Details of the formation of glycerol 3-phosphate from intermediates of glycolysis are shown in Figure 24-2. (PPP, pentose phosphate pathway TG, triacylglycerol FFA, free fatty acids VLDL, very low density lipoprotein.)...

Adipose tissue Storage and breakdown of triacylglyc-erol Esterification of fatty acids and lipolysis lipogenesis Glucose, lipoprotein triacylglycerol Free fatty acids, glycerol Lipoprotein lipase, hormone-sensitive lipase... 

Figure 7.3 The action of lipoprotein lipase in the hydrolysis of triacylglycerol in the blood and the fate of the fatty adds produced. Lipoprotein Lipase is attached to the luminal surface of the capillaries in the tissues that are responsible for removal of triacylglycerol from the bloodstream (e.g. adipose tissue, muscle, lactating mammary gland).

Hydrolysis of triacylglycerols is catalyzed by lipoprotein lipase, a membrane-bound enzyme located on the endothelium lining the capillary beds of the muscle and adipose tissue. 

Chylomicrons deliver tiiacylglycerols to tissues, where lipoprotein lipase releases free fatty acids for entry into cells. Triacylglycerols stored in adipose tissue are mobilized by a hormone-sensitive triacylglycerol lipase. The released fatty acids bind to serum albumin and are carried in the blood to the heart, skeletal muscle, and other tissues that use fatty acids for fuel. 

When the diet contains more fatty acids than are needed immediately as fuel, they are converted to triacylglycerols in the liver and packaged with specific apolipoproteins into very-low-density lipoprotein (VLDL). Excess carbohydrate in the diet can also be converted to triacylglycerols in the liver and exported as VLDLs (Fig. 21-40a). In addition to triacylglycerols, VLDLs contain some cholesterol and cholesteryl esters, as well as apoB-100, apoC-I, apoC-II, apoC-III, and apo-E (Table 21-3). These lipoproteins are transported in the blood from the liver to muscle and adipose tissue, where activation of lipoprotein lipase by apoC-II causes the release of free fatty acids from the VLDL triacylglycerols. Adipocytes take up these fatty acids, reconvert them to triacylglycerols, and store the products in intracellular lipid droplets myocytes, in contrast, primarily oxidize the fatty acids to supply energy. Most VLDL remnants are removed from the circulation by hepatocytes. The uptake, like that for chylomicrons, is... 

Decreased uptake of fatty acids In fasting, lipoprotein lipase activity of adipose tissue is low. Consequently, circulating triacyl-glycerol of lipoproteins is not available for triacylglycerol synthesis in adipose tissue. 

Chylomicrons transport dietary triacylglycerol and cholesteryl ester from the intestine to other tissues in the body. Very-low-density lipoprotein functions in a manner similar to the transport of endogenously made lipid from the liver to other tissues. These two types of triacylglycerol-rich particles are initially degraded by the action of lipoprotein lipase, an extracellular enzyme that is most active within the capillaries of adipose tissue, cardiac and skeletal muscle, and the lactating mammary gland. Lipoprotein lipase catalyzes the hydrolysis of triacylglycerols (see fig. 18.3). The enzyme is specifically activated by apoprotein C-II, which... 

Chylomicrons are synthesized in the intestine and transport dietary triacylglycerols to skeletal muscle and adipose tissue, and dietary cholesterol to the liver. At these target tissues the triacylglycerols are hydrolyzed by lipoprotein lipase on the surface of the cells and the released fatty acids are taken up either for metabolism to generate energy or for storage. The resulting cholesterol-rich chylomicron remnants are transported in the blood to the liver where they are taken up by receptor-mediated endocytosis. 

Correct answer = D. Clofibrate and gemfibrozil Increase the activity of lipoprotein lipase, thereby increasing the removal of VLDL from plasma. Niacin inhibits lipolysis in adipose tissue and thus eliminates the building blocks needed by the liver to produce triacylglycerol and there-... 

In the capillaries of adipose tissue and muscle, fatty acids of chylomicrons are removed from the triacylglycerols hy the action of lipoprotein lipase (LPL) LPL is present on the surface of the endothehal cells of the capillaries. Chylomicron apo-C-II activates LPL in the presence of phospholipid. 

The chylomicrons are released into the lymph system and then into the blood. These particles bind to membrane-bound lipoprotein lipases, primarily at adipose tissue and muscle, where the triacylglycerols are once again degraded into free... 

When the chylomicrons reach tissue cells the triacylglycerols are again hydrolyzed by lipoprotein lipase to fatty acids which can be taken up by the peripheral tissue cells. In adipose cells the fatty acids are then converted into fatty acyl CoA s and combined into triacylglycerols for storage. Alternatively tlie fatty acids can be broken down for energy using the various oxidative pathway in specific tissues. 

The triacylglycerols of chylomicrons and VLDL are hydrolyzed by lipoprotein lipase to fatty acids and glycerol. The fatty acids may be oxidized by various tissues. In adipose cells, the fatty acids are converted to triacylglycerols and stored. 

The storage of triacylglycerols in adipose tissue is mediated by insulin, which stimulates adipose cells to secrete lipoprotein lipase and to take up glucose, the source of glycerol for triacylglycerol synthesis. 

Fatty acids released by lipoprotein lipase are taken up by adipose cells and converted to triacylglycerols, but glycerol is not used because adipose tissue lacks glycerol kinase (see IV D 2 for pathway). 

Figure 6-9. Regulation of triacylglycerol stores in adipose tissue. Left = in the fed state. Right = in the fasted state. TG = triacylglycerol FA = fatty acid LPL = lipoprotein lipase DHAP = dihydroxyacetone phosphate = stimulated by circled TG = triacylglycerol of chylomicrons and VLDL.

C. VLDL levels are elevated because the decreased insulin and increased glucagon cause lipolysis of adipose triacylglycerols. The fatty acids and glycerol are repackaged in VLDL, which are secreted by the liver. Therefore, both triacylglycerols and cholesterol are elevated in the blood. Lipoprotein lipase is decreased because its synthesis and secretion by adipose tissue are stimulated by insulin. 

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