LDL and HDL
Low-density lipoproteins constitute a metabolic product that results after triglyceride is removed from very low density lipoproteins. This leaves a smaller, denser particle that primarily contains cholesteryl ester as its core lipid and a single protein called apoB. Cells throughout the body contain an LDL receptor that recognizes apoB. This allows the uptake of low-density lipoproteins into cells, supplying them with cholesterol. When sufficient low-density lipoproteins and cholesterol are available, cells use them in preference to synthesizing new cholesterol from precursors.

In contrast, high-density lipoproteins both deliver and remove cholesterol from tissues. In animals that have very little circulating low-density lipoproteins, such as rodents, high-density lipoproteins deliver cholesterol to steroid-producing tissues. Its major protein, apoAI, is made in both the intestine and the liver and is secreted with a small amount of lipid. These small HDL precursors of lecithin cholesterol acyl transferase (LCAT), thecholesterol is converted to cholesteryI ester-a process that makes it more hydrophobic and allows it to create a lipoprotein with a cholesteryl ester core. High density lipoproteins have at least one receptor, scavenger receptor B-1 (SRB-1). High density lipoproteins blind to SRB-1 in the liver and in adrenal cells; and via poorly understood process, cholesteryl ester, but not HDL protein, is transferred to cells. This process can supply cholesterol for steroid hormones and for bile. A plasma lipid transport protein called cholesteryl ester transfer protein (CETP) exchange cholesteryl ester in high-density lipoproteins for trigluceride in very low density lipoproteins, thus reducing the size and cholesterol content of high-density lipoproteins. CETP is not produced by rodents.
Lipoprotein(a)

Apo(a) is a large protein with homology to the blood-clothing protein plasminogen. Apo(a) complexes with low-density lipoproteins via a disulfide linkage and forms a lipoprotein called Lp(a). Lp(a) contains added protein and is denser than low-density lipoproteins.
Medical significance Blood levels of lipoproteins are major factors regulating risk for development of coronary artery atherosclerosis, the most common form of heart disease in the western world. Via unknown mechanisms, low-density lipoproteins and remnant lipoproteins infiltrate and then become attached to extracellular matrix molecules within the artery. Some of the lipoproteins are internalized by macrophages and smooth muscle cells.

This might first require chemical modification such as oxidation of the lipids. The resulting pathological findings are deposition of cholesterol in cells and matrix within the vessel wall, leading to a decrease in the diameter of the artery.
LDL cholesterol is a major predictor of the development of atherosclerosis in humans and in animals. Moreover, dietary and genetic modifications of animals have conclusively shown that elevated cholesterol in low-density lipoproteins or remnant lipoproteins is the only alteration required to convert a nonatherogenic animal into one that gets this disease.
In 'contrast, high-density lipoproteins appear to prevent atherosclerosis formation. The reasons are not entirely understood. Most likely, high-density lipoproteins remove excess cholesterol that accumulates in the artery, or high-­density lipoproteins prevent the oxidation of low-density lipoproteins.
Lp(a) levels are also correlated with the development of atherosclerosis. This relationship is most evident in Caucasian populations. Blood Lp(a) concentrations are primarily genetically determined; individuals with smaller forms of apo(a) produce a greater number of these molecules. Lp(a) particles may alter blood clotting or have alternative molecular interactions that make them more likely to accumulate in arteries. See also: Arteriosclerosis
Regulation of levels
Diet, exercise, and genetic factors control the levels of lipoproteins in the blood. Diets containing more cholesterol and saturated fats increase the amounts of LDL cholesterol. Lipoproteins containing primarily triglyceride are increased with obesity, diabetes, and intake of foods such as simple sugars and alcohol that are readily converted to triglyceride in the liver. Exercise lowers triglyceride.
HDL levels are increased by high cholesterol-high saturated fat diets, but low-density lipoproteins are increased at the same time. In addition, alcohol, oral' estrogen, and exercise raise high-density lipoproteins.
Lp(a) is reduced by estrogen.
Disorders
In most people the concentrations of blood lipoproteins are modulated by lifestyle and by poorly defined polygenetic factors. ApoB is produced in greater amounts in people with familial combined hyperlipoproteinemia. These people have increased very low density lipoproteins and low-density lipoproteins in their blood. Familial hypercholesterolemia is a disease due to a defect in removal of low-density lipoproteins from the bloodstream. This is either due to a defect in the LDL receptor or to a mutation in apoB that prevents low-density lipoproteins from being recognized by the receptor. Defects in lipoprotein lipase or its activator apoCII lead to very high blood levels of triglyceride. Defects in almost all the other apos and lipoprotein-metabolizing enzymes have been described and lead to diseases in humans.
Treatments .
A number of medical therapies have been developed to reduce blood concentrations of lipoproteins. Medications that reduce LDL cholesterol are effective in reducing atherosclerosis complications such as heart attacks and strokes. Bile acid-­binding resins reduce low-density lipoproteins by absorbing cholesterol in the gastrointestinal tract and augmenting its removal. The vitamin niacin decreases liver production of
very low density lipoproteins and low-density lipoproteins. HMG CoA reductase inhibitors, also known as statins, are inhibitors of the cholesterol synthesis in the liver. In turn, the liver increases the number of LDL receptors, leading to greater removal of low-density lipoproteins from the bloodstream.