Atherosclerosis, cholesterol/lipids

Number of Treatment Rabbits Serum Lipids (mg/dl) Atherosclerosis Cholesterol Triglycerides Arch Thoracic ... 

Atherosclerosis Common form of arteriosclerosis with deposits of yellow plaques containing cholesterol, lipid material within the intima and inner media of arteries. 

In 1913 Anitschkow showed that it was possible to establish atherosclerosis in rabbits by feeding cholesterol. Since then virtually all research on atherosclerosis has centered on cholesterol -circulating cholesterol and dietary cholesterol. The epidemiological data suggest a role for dietary fat, and hypercholesterolemia has been established as a principal risk factor for atherosclerosis. The lipid hypothesis was developed from the data obtained in the Framingham study, which suggested a curvilinear relationship between risk of atherosclerosis and plasma or serum cholesterol levels. However, studies of actual cholesterol intake as it affects cholesterol levels have yielded equivocal results. 

Cholesterol is biosynthesized in the liver trans ported throughout the body to be used in a va riety of ways and returned to the liver where it serves as the biosynthetic precursor to other steroids But cholesterol is a lipid and isn t soluble in water How can it move through the blood if it doesn t dis solve in if The answer is that it doesn t dissolve but IS instead carried through the blood and tissues as part of a lipoprotein (lipid + protein = lipoprotein) The proteins that carry cholesterol from the liver are called low density lipoproteins or LDLs those that return it to the liver are the high-density lipoproteins or HDLs If too much cholesterol is being transported by LDL or too little by HDL the extra cholesterol builds up on the walls of the arteries caus mg atherosclerosis A thorough physical examination nowadays measures not only total cholesterol con centration but also the distribution between LDL and HDL cholesterol An elevated level of LDL cholesterol IS a risk factor for heart disease LDL cholesterol is bad cholesterol HDLs on the other hand remove excess cholesterol and are protective HDL cholesterol IS good cholesterol... 

Thus, it is apparent that soya, some soya products and linseed oil influence blood lipid levels, particularly cholesterol and LDL cholesterol. While the extent of the reduction appears to largely depend on an individual s initial serum cholesterol level, the maximum reductions observed are of the order of 10-15%. For hyperlipidemic individuals this may not be a marked reduction, but such an effect on the general population may well have a beneficial effect on the overall incidence of cardiovascular disease and atherosclerosis. The possibility that non-phytoestrogenic dietary components may contribute to the hypocholes-terolemic properties cannot, however, be discounted. Indeed, certain types of dietary fibre have been shown to have a hypolipidemic effect via their ability to increase faecal excretion rates. 

An increase in serum lipids is believed to contribute to or cause atherosclerosis, a disease characterized by deposits of fatty plaques on the inner walls of arteries. These deposits result in a narrowing of the lumen (inside diameter) of the artery and a decrease in blood supply to the area served by the artery. When these fatty deposits occur in the coronary arteries, the patient experiences coronary artery disease. Lowering blood cholesterol levels can arrest or reverse atherosclerosis in the vessels and can significantly decrease the incidence of heart disease. 

While cholesterol is believed to be chiefly concerned in the relationship, other serum lipids such as triacylglycerols may also play a role. Atherosclerosis is character-... 

Zhao, C. et al.. Effects of commercial anthocyanin-rich extracts on colonic cancer and nontumorigenic colonic cell growth, J. Agric. Food Chem., 52, 6122, 2004. Kaplan, M. et al.. Pomegranate juice supplementation to atherosclerotic mice reduces macrophage lipid peroxidation, cellular cholesterol accumulation and development of atherosclerosis, J. Nutr, 131, 2082, 2001. 

The development of CHD is a lifelong process. Except in rare cases of severely elevated serum cholesterol levels, years of poor dietary habits, sedentary lifestyle, and life-habit risk factors (e.g., smoking and obesity) contribute to the development of atherosclerosis.3 Unfortunately, many individuals at risk for CHD do not receive lipid-lowering therapy or are not optimally treated. This chapter will help identify individuals at risk, assess treatment goals based on the level of CHD risk, and implement optimal treatment strategies and monitoring plans. 

Atherosclerosis is a wide-spread pathology, manifested chiefly by the deposition of cholesterol in arterial walls, which results in the formation of lipid plaques (atheromas). Lipid plaques are specific foreign bodies around which the connective tissue develops abnormally (this process is called sclerosis). This leads to the cal-cification of the impaired site of a blood vessel. The blood vessels become inelastic and compact, the blood supply through the vessels is impeded, and the plaques may develop into thrombi. 

Contrary to LDL, high-density lipoproteins (HDL) prevent atherosclerosis, and therefore, their plasma levels inversely correlate with the risk of developing coronary artery disease. HDL antiatherogenic activity is apparently due to the removal of cholesterol from peripheral tissues and its transport to the liver for excretion. In addition, HDL acts as antioxidants, inhibiting copper- or endothelial cell-induced LDL oxidation [180], It was found that HDL lipids are oxidized easier than LDL lipids by peroxyl radicals [181]. HDL also protects LDL by the reduction of cholesteryl ester hydroperoxides to corresponding hydroperoxides. During this process, HDL specific methionine residues in apolipoproteins AI and All are oxidized [182]. 

The expression of 15-LOX in atherosclerotic lesions is one of the major causes of LDL oxidative modification during atherosclerosis. To obtain the experimental evidence of a principal role of 15-LOX in atherosclerosis under in vivo conditions, Kuhn et al. [67] studied the structure of oxidized LDL isolated from the aorta of rabbits fed with a cholesterol-rich diet. It was found that specific LOX products were present in early atherosclerotic lesions. On the later stages of atherosclerosis the content of these products diminished while the amount of products originating from nonenzymatic lipid peroxidation increased. It was concluded that arachidonate 15-LOX is of pathophysiological importance at the early stages of atherosclerosis. Folcik et al. [68] demonstrated that 15-LOX contributed to the oxidation of LDL in human atherosclerotic plaques because they observed an increase in the stereospecificity of oxidation in oxidized products. Arachidonate 15-LOX is apparently more active in young human lesions and therefore, may be of pathophysiological importance for earlier atherosclerosis. In advanced human plaques nonenzymatic lipid peroxidation products prevailed [69],... 

Marsh MM, Walker VR, Curtiss LK, Banka CL (1999) Protection against atherosclerosis by estrogen is independent of plasma cholesterol levels in LDL receptor-deficient mice. J Lipid Res 40 893-900... 

Erotein whether or not cholesterol was added to the diets C3) ince the publication of this experiment over 45 years ago, there has been a recent resurgence of interest in the area of protein effects on plasma lipids and atherosclerosis. This paper summarizes some of the data generated in our laboratory over the last several years and discusses their significance in relation to hypercholesterolemia and atherosclerosis in other species including humans. 

The standard diet used in our experiments is a semipurified, cholesterol-free preparation that is composed of 25% protein, 40% sucrose, 13% coconut oil, 1% corn oil, 15% cellulose, 5% mineral mix, and 1% vitamin mix. This diet has been shown to induce an endogenous hypercholesterolemia and lead to atherosclerosis in rabbits and monkeys (4, 5). The specific question addressed by our series of investigations is whether the type of dietary protein, when all other dietary components are constant, can influence the development of hyperlipoproteinemia and atherosclerosis. More specifically, we have examined the effects of the individual amino acids, lysine and arginine, and their ratios in the diet on plasma and hepatic lipids as well as the development of arterial plaques. 

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