Download Cholesterol Transport Systems and Their Relation to by J. Shepherd, C. J. Packard (auth.), Dr. med. Armin PDF

By J. Shepherd, C. J. Packard (auth.), Dr. med. Armin Steinmetz, Professor Dr. med. Hans Kaffarnik, Professor Dr. med. Jürgen Schneider (eds.)

A variety of medical and epidemiological reviews have proven that problems of lipoprotein metabolism represent the most vital chance elements for the improvement of atherosclerosis and heart affliction. This quantity examines the cutting-edge of lipoprotein subclass metabolism and its relation to those ailments. The authors additionally document on new advancements in regards to the position of lipoprotein recptors, macrophages and apolipoprotein E polymorphism in ldl cholesterol homeostasis. the combo of normal define shape and extremely particular points of ldl cholesterol shipping will curiosity these in different disciplines following advancements within the box, in addition to these at once interested by lipoprotein research.

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Extra resources for Cholesterol Transport Systems and Their Relation to Atherosclerosis

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Especially in patients with familial hypercholesterolemia (FH), there are elevations of serum LDL cholesterol level and premature coronary atherosclerosis, because of decreased activity or deficiency of the LDL receptor [4, 5]. If the number of hepatic LDL receptors decreases due to dietary factors such as casein [6], cholesterol [7], or animal fats [8], the serum level of cholesterol (LDL cholesterol) increases in experimental animals or even in the normal population [2], and atherosclerosis develops.

J Clin Invest 78: 1206-1219 . 25. Nestruck AC, Bouthillier D, Sing CF, Davignon J (1987) Apolipoprotein E polymorphism and plasma cholesterol response to probucol. Metabolism 36: 743-747 Regulation of Macrophage Cholesterol Homeostasis G. SCHMITZ, B. BRENNHAUSEN, and H. ROBENEK Lipoprotein receptors playa major role in the homeostasis of plasma lipoproteins. They are integrated constituents of cell membranes and bind certain lipoproteins which are then internalized by the cells. Insofar as lipoprotein receptors affect the concentration of lipoproteins in the plasma and may play a role in lipoprotein accumulation in arterial cells, they have both a direct and an indirect influence on the progression of atherosclerosis.

The mechanism by which such a cellular defect could cause an increase in the concentrations of LDL apo B is not clear. M. Grundy et al. Animal Model for Familial Combined Hyperlipidemia Until now, an animal model has not been found that might facilitate the study of the defect in FCRL at a molecular level. Recently, a spontaneous genetic mutation in rabbits which has many features of FCRL has been noted. Affected animals have increased levels of VLDL and/or LDL and a predisposition to atherosclerosis.

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