INFLUENCE OF LIPOLYSIS ON CHYLOMICRON CLEARANCE AND HDL CHOLESTEROL LEVELS

Atherogenic risk is accurately defined by the turnover of the lipoprot ein classes that transport cholesterol and triglycerides, and by the a polipoproteins that determine the fate of these particles. Post-prandi al triglyceride levels have also been shown to be an accurate predicto r of atherogenic risk. The post-prandial triglyceride levels and conve rsion of very low density lipoprotein (VLDL) to intermediate density l ipoprotein (IDL) are controlled by a dynamic metabolic process involvi ng lipoprotein lipase (LPL) and hepatic lipase. The interaction betwee n the two enzymes modulates triglyceride transport through the plasma and influences the structure and serum concentrations of the denser ch olesterol-rich low density lipoproteins (LDL) and high density lipopro teins (HDL). Inadequate LPL function, a consequence either of impaired enzyme function or simply post-prandial overloading, can have profoun d pathophysiological consequences. High levels of large HDL2 reflect e ffective catabolism of triglyceride-rich lipoproteins by LPL whereas l ow levels of this lipoprotein reflect inadequate LPL activity or eleva ted hepatic lipase activity. Individuals with low levels of HDL2 are p rone to coronary artery disease. Overloading of LPL can occur in insul in resistance due to the absence of normal insulin-mediated suppressio n of VLDL secretion and the consequence is hypertriglyceridaemia. In a ddition, a deficiency in LPL can arise from a genetic defect which, in the homozygous state, results in pronounced hypertriglyceridaemia and pancreatitis. The correct management for patients with inadequate LPL activity is to optimize triglyceride metabolism, particularly in the post-prandial state.