ABSTRACT
Some evidence exists that it may be important in the release of cholesteryl ester from HDL molecules circulating through the liver (see page 46). As such, it may allow the regeneration of the smaller HDL3 from HDL2. This HDL3 may then be released back into the systemic circulation to acquire further cholesterol, and so on in a cyclical process, allowing the return of cholesterol to the liver. This may explain why, despite the inverse relationship between post-heparin plasma hepatic lipase activity and HDL cholesterol, particularly HDL2 cholesterol, there is no unconfounded evidence that hepatic lipase activity is related to the risk of CHD. Hepatic lipase also appears to be important in the conversion of smaller VLDL particles to LDL through the intermediary of IDL. In hepatic lipase deficiency there is an accumulation of βVLDL (or IDL-like particles) in the circulation similar to that in type III hyperlipoproteinaemia (see Chapter 7), and despite the hypertriglyceridaemia present in the patients so far described, HDL cholesterol levels are high. In the converse situation, when hepatic lipase activity is high, there is a tendency for smaller, less buoyant LDL particles to be generated. This fits well with the concept that CETP removes cholesteryl ester from larger LDL particles in exchange for triglyceride. Smaller, dense LDL particles would then be formed when hepatic lipase removes this triglyceride from LDL. Androgens increase hepatic lipase activity, and this might at least partly explain the greater tendency for smaller, dense LDL and low HDL cholesterol in men compared with women. Polymorphisms conferring decreased hepatic lipase activity are prevalent in Afro-Americans and those associated with increased hepatic lipase activity are common in Turkey, and these offer probable explanations for the relatively high and low HDL cholesterol levels, respectively, in these two populations.
