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 reports have proven that issues of lipoprotein metabolism represent the most vital chance components for the improvement of atherosclerosis and heart affliction. This quantity examines the state-of-the-art of lipoprotein subclass metabolism and its relation to those illnesses. The authors additionally document on new advancements about the function of lipoprotein recptors, macrophages and apolipoprotein E polymorphism in ldl cholesterol homeostasis. the combo of common define shape and extremely particular features of ldl cholesterol shipping will curiosity these in different disciplines following advancements within the box, in addition to these at once enthusiastic about lipoprotein research.
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Additional info for Cholesterol Transport Systems and Their Relation to Atherosclerosis
This overproduction can be manifested as increased plasma levels of VLDL, IDL, LDL, or apo B alone. While the best therapeutic regime is not known for certain, several possible approaches that can correct the abnormalities in plasma lipoprotein levels are available. Most participants agreed that nicotinic acid is the drug of choice with or without bile acid sequestrants, but difficulty with nicotinic acid by some patients prevents its use. Some participants believed that bile acid sequestrants alone or in combination with fibric acids or mevinolin can have a role in treatment of the specific forms of hyperlipidemia often present in this condition.
These nutrients appear to increase the synthesis of VLDL triglyceride, but they seemingly do not promote the formation of VLDL apo B. Consequently, restriction of carbohydrate and alcohol may have little beneficial effect on the underlying defect of FCRL. Another dietary constituent that affects the synthesis ofVLDL triglyceride is omega-3 fatty acids. Large amounts of dietary fish oil containing omega-3 fatty acids can profoundly reduce plasma triglycerides in hypertriglyceridemic subjects due to a variety of causes.
Arteriosclerosis 8: 1-21 8. Sing CF, Davignon J (1985) Role of the apolipoprotein E polymorphism in determining normal plasma lipid and lipoprotein variation. Am J Hum Genet 37: 268-285 9. Utermann G, Jaeschke M, Menzel J (1975) Familial hyperlipoproteinemia type III: deficiency of a specific apolipoprotein (apo E-III) in the very low density lipoproteins. FEBS Lett 56: 352-355 10. Utermann G, Vogelberg KH, Steinmetz A, Schoenborn W, Pruin N, J aeschke M, Hees M (1979) Polymorphism of apolipoprotein E.
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