Lipoproteins Metabolism

          Plasma lipoprotein are in a dynamic state. Their continuous synthesis and degradation are accompanied by rapid exchanges of lipid and protein components between the different lipoprotein classes. Major sites of plasma lipoprotein synthesis are liver and intestine. The necessary components are triacylglycerols, cholesterol (and cholesterol esters), phospholipids and apoproteins. Three enzymes play an important role in the delivery, storage and mobilization of lipoproteins and cholesterol:

1. Lipoprotein lipase (LPL): LPL is the major enzyme involved in the hydrolysis of triacylglycerols of chylomicrons and VLDL releasing fatty acids and glycerol. Both phospholipids and Apo C11 are required as cofactors for LPL activity.

     Insulin increases LPL activity in adipose tissue (but not in muscles) So after a meal, insulin released promotes fuel storage as triacylglycerols in adipose tissue. During starvation, activity of LPL in adipose tissue is low whereas activity of the heart enzyme is high. FFA released from VLDL are used by the heart as a fuel.

- In general, LPL has different functions in different tissues:

• In lactating breast it stimulates triacylglycerol synthesis for milk fat.
• In adipose tissue it promotes fuel storage.
• In cardiac and skeletal muscles (low K m) it provides energy.

1. Hepatic lipase: Its role is not completely clear. However it continues lipolysis of IDLs in their stepwise conversion to LDL. Hepatic lipase also hydrolyses HDL – triacylglycerols.
2. Lecithin cholesterol acyl transferase (LCAT): LCAT ia a plasma enzyme synthesized in liver. It circulates in plasma with HDL and LDL. The substrate for LCAT is phosphatidylcholine, lecithin (a component of phospholipids bilayer of HDL). Apo A1 which is associated with HDL is a powerful activator of LCAT. LCAT catalyzes the following reversible reaction:                        

      This reaction is responsible for formation of cholesterol esters in plasma. So, LCAT plays a significant role in removal of cholesterol from the circulating lipoproteins similar to the role of LPL in removal of triacylglycerol from chylomicrons and VLDL.