Genetic defects in lipoprotein metabolism: elevation of atherogenic lipoproteins caused by impaired catabolism

Article Abstract:

The proteins, apolipoprotein B and E, are located on the surface of lipoprotein molecules, which are fat and protein compounds. These apolipoproteins are involved in the binding of cholesterol-containing particles to specific lipoprotein attachment sites on cells, called receptors. This process is an important pathway for controlling the blood levels of cholesterol. An increase in blood levels of certain lipoproteins may contribute to the development of atherosclerosis, a blood vessel disorder in which lipids accumulate and cells proliferate within the arteries. Three types of lipoprotein metabolism disorders may contribute to the rise in atherogenic lipoproteins (lipoproteins that may cause atherosclerosis). Type III hyperlipoproteinemia results from certain mutations in apolipoprotein E, thereby preventing the binding of portions of very-low-density-lipoprotein (VLDL) and chylomicrons (small fat particles in the blood). Type III hyperlipoproteinemia associated with elevated levels of VLDL remnants leads to the development of atherosclerosis. The substitution of a single amino acid in apolipoprotein B prevents low-density lipoprotein (LDL) from binding to its receptor, resulting in increased blood cholesterol levels and a disorder called familial defective apolipoprotein B-100. The third disorder, familial hypercholesterolemia, is associated with increased LDL levels and the early development of atherosclerosis. It results from several mutations of the LDL receptor that interfere with the binding of LDL to its receptor. These genetic defects in lipoprotein metabolism contribute to the understanding of mechanisms responsible for normal lipoprotein metabolism and role of lipoproteins in atherosclerosis. (Consumer Summary produced by Reliance Medical Information, Inc.)

Genetic aspects, Lipid metabolism, Lipoproteins

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Long-term Exercise and Atherogenic Activity of Blood Mononuclear Cells in Persons at Risk of Developing Ischemic Heart Disease

Article Abstract:

Regular exercise appears to lower the risk of heart disease by decreasing blood levels of immune system chemicals that promote atherosclerosis and increasing levels of chemicals that prevent atherosclerosis. Researchers measured blood levels of several immune system chemicals called cytokines in 43 men and women before and after they engaged in a regular exercise program for six months. After six months, levels of cytokines that promote atherosclerosis dropped 58% and those that prevent atherosclerosis increased 36%. The more the person exercised, the greater the changes. This may explain why physical activity protects against coronary artery disease.

Prevention, Exercise, Exercise physiology, Cytokines

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Effect of glucose-insulin-potassium infusion on mortality in patients with acute ST-segment elevation myocardial infarction

Article Abstract:

The effect of high-dose glucose-insulin-potassium (GIK) infusion on mortality in patients with acute ST-segment elevation myocardial infarction (STEMI) is determined. The results state that high-dose GIK infusion had a neutral effect on mortality, cardiac arrest, and cardiogenic shock in patients with acute STEMI.

Causes of, Risk factors, Influence, Heart attack, Insulin, Glucose, Dextrose

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