Lipid Use by the Tissues

Most of the TAG contained in chylomicrons is broken down in the capillary beds of skeletal and cardiac muscle and adipose tissue.

The TAG is degraded to FFA and glycerol by lipoprotein lipase (LPL). This enzyme is synthesized and secreted primarily by adipocytes and muscle cells. Secreted LPL is anchored to the luminal surface of endothelial cells in the capillaries of muscle and adipose tissues. [Note: Familial chylomicronemia (type I hyperlipoproteinemia) is a rare, autosomal-recessive disorder caused by a deficiency of LPL or its coenzyme apo C-II . The result is fasting chylomicronemia and severe hypertriacylglycerolemia, which can cause pancreatitis.]
1. Fate of free fatty acids: The FFA derived from the hydrolysis of TAG may either directly enter adjacent muscle cells and adipocytes or be transported in the blood in association with serum albumin until they are taken up by cells. [Note: Human serum albumin is a large protein secreted by the liver. It transports a number of primarily hydrophobic compounds in the circulation, including FFA and some drugs.] Most cells can oxidize FA to produce energy . Adipocytes can also reesterify FFA to produce TAG molecules, which are stored until the FA are needed by the body .
2. Fate of glycerol: Glycerol released from TAG is taken up from the blood and phosphorylated by hepatic glycerol kinase to produce glycerol 3-phosphate, which can enter either glycolysis or gluconeogenesis by oxidation to dihydroxyacetone phosphate (see p. 101) or be used in TAG synthesis .
3. Fate of chylomicron remnants: After most of the TAG has been removed, the chylomicron remnants (which contain cholesteryl esters, phospholipids, apolipoproteins, fat-soluble vitamins, and a small amount of TAG) bind to receptors on the liver (apo E is the ligand) and are endocytosed. The intracellular remnants are hydrolyzed to their component parts. Cholesterol and the nitrogenous bases of phospholipids (for example, choline) can be recycled by the body. [Note: If removal of remnants by the liver is decreased because of impaired binding to their receptor, they accumulate in the plasma. This is seen in the rare type III hyperlipoproteinemia (also called familial dysbetalipoproteinemia or broad beta disease).]