Intermediate density lipoproteins (IDL) consist of cholesterol esters, which are posthepatic remnants derived from dietary sources. Metabolites of IDL are transient lipoproteins measured only in certain pathologic conditions.
Low-density lipoprotein (LDL) is mainly composed of the cholesterol ester and is associated with B-100 apoprotein. LDL cholesterol is approximately 60% to 70% of total cholesterol. Elevated levels of LDL cholesterol are associated with increased myocardial infarction in women older than 65 years of age. There is a structural class called LDL (a ) that is associated with myocardial infarction.
High-density lipoprotein (HDL) is composed of cholesterol esters with apoproteins A-I and A-II. These particles are 20% to 30% of total cholesterol and are the most dense.
Metabolism Cholesterol metabolism is divided into two pathways: (i) the exogenous pathway derived from dietary sources, and (ii) the endogenous pathway or the lipid transport pathway. Individuals vary in their ability to metabolize cholesterol, with patients classified as normals, hyporesponders, and hyperresponders (29). Hyporesponders may be given cholesterol-loaded diets with no effect on serum cholesterol measurements. Hyperresponders, in contrast, have high serum cholesterol levels, regardless of dietary intake. Explanations for these differences are well described in animal models, but not in humans.
When a meal is eaten, cholesterol is transported as dietary fat. The average daily American diet contains approximately 100 g of triglyceride and approximately 1 g of cholesterol. Triglycerides are found in the core lipoprotein particles and are removed through the capillary endothelium and the chylomicron. Theories suggest that hypo-and hyperresponses to dietary cholesterol may occur secondary to the liver’s ability to recognize and metabolize apoprotein E. In the animal model, populations with large numbers of liver receptors for apoprotein E easily metabolize cholesterol and are labeled hyporesponders. Individuals with a reduced number of apoprotein E receptors are unable to metabolize cholesterol as readily, which increases the number of lipid particles. These individuals are considered hyperresponders. Despite dietary cholesterol modification, these individuals continue to have high serum cholesterol levels.
After metabolic degradation of dietary chylomicrons, apoprotein substitution occurs and liver metabolism of cholesterol esters begins. Lipid transport is now in the endogenous pathway. Carbohydrates are synthesized to fatty acids and esterified with glycerol to form triglycerides. These newly formed triglycerides are not of dietary origin and are placed in the core of VLDL. These particles are relatively large and carry five to ten times more triglyceride than cholesterol esters with apoprotein B-100. Hypertriglyceridemia is an independent risk factor for cardiovascular disease. The relationship between hypertriglyceridemia and cardiovascular disease is well known but poorly defined.
VLDL particles are transported to tissue capillaries, where they are broken down to usable fuels, monoglycerides, and fatty acids. After metabolic enzymatic degradation in the peripheral tissues, IDL remains and is either catabolized in the liver by binding to LDL receptors or modified in the peripheral tissues. As noted previously, they are associated with apoprotein E receptors, the liver recognition receptors. The LDL cholesterol, or the so-called high-risk cholesterol, is found in high circulating levels.