Atherogenic

The reason for the cholesterol-lowering effect of polyunsaturated fatty acids is still not fully understood. It is clear, however, that one of the mechanisms involved is the up-regulation of LDL receptors by poly-and monounsaturated as compared with saturated fatty acids, causing an increase in the catabolic rate of LDL, the main atherogenic lipoprotein. In addition, saturated fatty acids cause the formation of smaller VLDL particles that contain relatively more cholesterol, and they are utilized by extrahepatic tissues at a slower rate than are larger particles—tendencies that may be regarded as atherogenic. 

BHAKDi s (1998) Atherogenic properties of enzymatically degraded LDL selective induction of MCP-1 and cytotoxic effects on human macrophages Arteriosclerosis, Thrombosis and Vascular Biology 18, 1376-85. 

KAPLAN M and AVIRAM M (1999) Oxidized low density lipoprotein atherogenic and proinflammatoiy characteristics during macrophage foam cell formation. An inhibitory role for nutritional antioxidants and serum paraoxonase Clinical Chemistry Laboratory Medicine 37,111-9,1. 

PORKKALA-SARATAHO E K, NYYSSONEN K M, KAIKKONEN J E, POULSEN H E, HAYN E M, SALONEN R M, SALONEN J T (1998) A randomized, single-blind, placebo controlled trial of the effects of 200 mg a-tocopherol on the oxidation resistance of atherogenic hpoproteins, American Journal of Clinical Nutrition, 68, 1034-41. 

Although atherosclerosis and rheumatoid arthritis (RA) are distinct disease states, both disorders are chronic inflammatory conditions and may have common mechanisms of disease perpetuation. At sites of inflammation, such as the arterial intima undergoing atherogen-esis or the rheumatoid joint, oxygen radicals, in the presence of transition-metal ions, may initiate the peroxidation of low-density lipoprotein (LDL) to produce oxidatively modified LDL (ox-LDL). Ox-LDL has several pro-inflammatory properties and may contribute to the formation of arterial lesions (Steinberg et /., 1989). Increased levels of lipid peroxidation products have been detected in inflammatory synovial fluid (Rowley et /., 1984 Winyard et al., 1987a Merry et al., 1991 Selley et al., 1992 detailed below), but the potential pro-inflammatory role of ox-LDL in the rheumatoid joint has not been considered. We hypothesize that the oxidation of LDL within the inflamed rheumatoid joint plays a pro-inflammatory role just as ox-LDL has the identical capacity within the arterial intima in atherosclerosis. 

NF-xB activation has been linked with atherosclerosis (Andalibi etal., 1993 Liao etui., 1993). Mice that were maintained on an atherogenic diet, which resulted in ox-LDL accumulation in the liver and arteries, showed NF-xB activation in hepatic tissues. Furthermore, inflammatory gene up-regulation corresponded to the concentration of accumulated lipid peroxides as well as genetic susceptibility to fetty-streak development. 

Kume, N., Cybulsky, M.I. and Gimbrone, M.A. (1992). Lysophosphatidylcholine, a component of atherogenic lipoproteins, mediates mononuclear leucocyte adhesion in cultured human and rabbit endothelial cells. J. Clin. Invest. 90, 1138-1144. 

Fatty acids play an important role as a risk factor for cardiovascular diseases, that is by forming plaques within the arteria. Low density lipoproteins (LDL) are seen as the most important risk factor. In the clinical chemistry laboratory, both LDLs and HDLs (high density lipids, considered as an anti-atherogenic factor) are determined. 

Shift LDL cholesterol particle size from predominantly small, dense, highly atherogenic particles to larger, less atherogenic particles. 

After assessment and control of LDL cholesterol, patients with serum triglycerides of 200 to 499 mg/dL (2.26 to 5.64 mmol/L) should be assessed for atherogenic dyslipidemia (low HDL cholesterol and increased small-dense LDL particles) and metabolic syndrome. 

Patients with metabolic syndrome are twice as likely to develop type 2 diabetes and four times more likely to develop CHD.3,11 These individuals are usually insulin resistant, obese, have hypertension, are in a prothrombotic state, and have atherogenic dyslipidemia characterized by low HDL cholesterol and elevated triglycerides, and an increased proportion of their LDL particles are small and dense.3... 

In addition to the five major risks, the ATP III guidelines recognize other factors that contribute to CHD risk. These are classified as life-habit risk factors and emerging risk factors. Life-habit risk factors, consisting of obesity, physical inactivity, and an atherogenic diet, require direct intervention. For example, emerging risk factors are lipoprotein(a), homocysteine, prothrombotic/proinflammatory factors, and C-reactive protein (CRP). C-reactive protein is a marker of low-level inflammation and appears to help in... 

De Waard B et al. Serial analysis of gene expression to assess the endothelial cell response to an atherogenic stimulus. Gene 1999 226 1-8. 

Hayashi K, Kurushima H, Kuga Y, Shingu T, Tanaka K, Yasunobu Y, et al. Comparison of the effect of bezafibrate on improvement of atherogenic lipoproteins in Japanese familial combined hy-perlipidemic patients with or without impaired glucose tolerance. Cardiovasc Drugs Ther 1998 12 3-12. 

The most clear-cut effects are anti-bacterial, anti-oxidant, anti-atherogenic, anti-cancer and immunostimulatory. 

Omoni AO and Aluko RE. 2005. The anti-carcinogenic and anti-atherogenic effects of lycopene a review. Trends Food Sci Technol 16(8) 344—350. 

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