A large proportion of LDL cholesterol is in the form of esters containing saturated fatty acids, whereas HDL contains unsaturated fatty acids. HDL lipoproteins tend to transport excess cholesterol from peripheral tissues back to the liver where it is broken down. HDL is assembled from apolipoprotein-AI, phospholipid, and free cholesterol discs secreted by the liver and intestines. The free cholesterol is esterified in the mature HDL and can then be transferred to LDL or taken up by the liver or steroid-metabolising tissues.
In contrast, LDL particles are involved in the uptake of cholesterol into tissue cells via a receptor-mediated process. A decrease in the number of LDL receptors on tissue cells has been linked to high circulating levels of plasma cholesterol. Decreased receptors means decreased cholesterol uptake and the raised LDL levels that ensue increase the risk of atheroma. About 20 years ago it was discovered that mutations in the gene that encodes the LDL receptor protein causes familial hypercholesterolaemia. In this condition there are high levels of LDL but tissue cells are unable to take up cholesterol from the blood. People affected by this mutation are at a much higher risk of coronary heart disease and stroke than other people (Brown 1984).
Several factors can influence the levels of circulating HDL (Scott, 1999). For example, there is a difference in levels between women and men: women have higher levels of HDL than men up until the menopause, and this offers them some protection against heart disease. Levels of HDL can also be increased by exercise, weight loss, moderate alcohol intake, and chemicals such as fibric acid derivatives, nicotinic acid, and tamoxifen.
(published with permission in writing from:http://www.nurseminerva.co.uk/)
