Low density lipoproteins - carry cholesterol from the liver to cells of the body. Sometimes referred to as the "bad cholesterol" lipoprotein.
High density lipoproteins - collects cholesterol from the body's tissues, and brings it back to the liver. Sometimes referred to as the "good cholesterol" lipoprotein.
Because LDLs transport cholesterol to the arteries and can be retained there by arterial proteoglycans starting the formation of plagues, increased levels are associated with atherosclerosis, and thus heart attack, stroke and peripheral vascular disease. This is why cholesterol inside LDL lipoproteins is called bad cholesterol. Still, it is not the cholesterol that is bad; it is instead how and where it is being transported, and in what amounts over time.
Increasing evidence has revealed that the concentration and size of the LDL particles more powerfully relates to the degree of atherosclerosis progression than the concentration of cholesterol contained within all the LDL particles. The healthiest pattern, though relatively rare, is to have small numbers of large LDL particles and no small particles. Having small LDL particles, though common, is an unhealthy pattern; high concentrations of small LDL particles (even though potentially carrying the same total cholesterol content as a low concentration of large particles) correlates with much faster growth of atheroma, progression of atherosclerosis and earlier and more severe cardiovascular disease events and death.
LDL is formed as VLDL lipoproteins, which lose triglyceride through the action of lipoprotein lipase (LPL), and become smaller and denser containing a higher proportion of cholesterol.
A hereditary form of high LDL is familial hypercholesterolemia (FH). Increased LDL is termed hyperlipoproteinemia type II (after the dated Fredrickson classification).
LDL poses a risk for cardiovascular disease when it invades the endothelium and becomes oxidized since the oxidized form is more easily retained by the proteoglycans. A complex set of biochemical reactions regulates the oxidation of LDL, chiefly stimulated by presence of free radicals in the endothelium. Nitric oxide down-regulates this oxidation process catalyzed by L-arginine. Correspondingly when there are high levels of asymmetric dimethylarginine in the endothelium, production of nitric oxide is inhibited and more LDL oxidation occurs.
High density lipoproteins - collects cholesterol from the body's tissues, and brings it back to the liver. Sometimes referred to as the "good cholesterol" lipoprotein.
Because LDLs transport cholesterol to the arteries and can be retained there by arterial proteoglycans starting the formation of plagues, increased levels are associated with atherosclerosis, and thus heart attack, stroke and peripheral vascular disease. This is why cholesterol inside LDL lipoproteins is called bad cholesterol. Still, it is not the cholesterol that is bad; it is instead how and where it is being transported, and in what amounts over time.
Increasing evidence has revealed that the concentration and size of the LDL particles more powerfully relates to the degree of atherosclerosis progression than the concentration of cholesterol contained within all the LDL particles. The healthiest pattern, though relatively rare, is to have small numbers of large LDL particles and no small particles. Having small LDL particles, though common, is an unhealthy pattern; high concentrations of small LDL particles (even though potentially carrying the same total cholesterol content as a low concentration of large particles) correlates with much faster growth of atheroma, progression of atherosclerosis and earlier and more severe cardiovascular disease events and death.
LDL is formed as VLDL lipoproteins, which lose triglyceride through the action of lipoprotein lipase (LPL), and become smaller and denser containing a higher proportion of cholesterol.
A hereditary form of high LDL is familial hypercholesterolemia (FH). Increased LDL is termed hyperlipoproteinemia type II (after the dated Fredrickson classification).
LDL poses a risk for cardiovascular disease when it invades the endothelium and becomes oxidized since the oxidized form is more easily retained by the proteoglycans. A complex set of biochemical reactions regulates the oxidation of LDL, chiefly stimulated by presence of free radicals in the endothelium. Nitric oxide down-regulates this oxidation process catalyzed by L-arginine. Correspondingly when there are high levels of asymmetric dimethylarginine in the endothelium, production of nitric oxide is inhibited and more LDL oxidation occurs.
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