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Atherosclerosis fatty acids

PPARa Liver, heart, skeletal muscle, atherosclerotic lesions TG- and LDL-C-lowering and HDL-C-raising re-directs excess cholesterol from the peripheral tissues to the liver for excretion into the bile via HDL-C slowed progression of atherosclerosis Fatty acids, eico-sanoids (fatty acids derived from FAS ) Fibrates fenofibrate (Tricor ), genfibrozil (Lopid ) Dyslipidemia... [Pg.945]

PPARy White adipose tissue, atherosclerotic lesions Insulin-sensitizing and glucoselowering re-directs TG from non-adipose tissues and visceral adipose depots for storage in subcutaneous adipose tissue slowed progression of atherosclerosis Fatty acids, eico-sanoids Th iazolid i ned iones pioglitazone (Actos ), rosiglita-zone (Avandia ) Type 2 diabetes, (insulin resistance, metabolic syndrome)... [Pg.945]

The state of knowledge in the early 1990s of the effects of fat on health lacks clarity and general agreement. There is great support for the thesis that fully saturated fats are associated with problems of atherosclerosis and arterial fatty deposit, but there is evidence that stearates, which are saturates, are only poorly utilized in human digestion. Another body of work has estabUshed a connection between unsaturated fatty acids and a better state of arterial health and lowered fat body attachment to the arterial wall (23) contrary evidence exists that highly unsaturated fats polymerize more readily and thus contribute to arterial plaque formation. [Pg.117]

Atherosclerosis is a degenerative disease which is characterized by cholesterol-containing thickening of arterial walls. Saturated fatty acids, high levels of cholesterol, elevated blood pressure, and elevated serum lipoprotein are well-knowm risk... [Pg.297]

PPAR5 Ubiquitous Potent TG- and LDL-C-lowering and potent HDL-C-raising increased oxidative disposal of fatty acids in adipose and skeletal muscle thermogenesis weight loss Fatty acids, eicosanoids (fatty acids derived from VLDL particles ) GW501516 currently in Phase II clinical trials Dyslipidemia, obesity atherosclerosis ... [Pg.945]

One major prerequisite for the maintenance of health is that there be optimal dietary intake of a number of chemicals the chief of these are vitamins, certain amino acids, certain fatty acids, various minerals, and water. Because much of the subject matter of both biochemistry and nutrition is concerned with the smdy of various aspects of these chemicals, there is a close relationship between these two sciences. Moreover, more emphasis is being placed on systematic attempts to maintain health and forestall disease, ie, on preventive medicine. Thus, nutritional approaches to—for example—the prevention of atherosclerosis and cancer are receiving increased emphasis. Understanding nutrition depends to a great extent on a knowledge of biochemistry. [Pg.2]

Small amounts of trans-unsamrated fatty acids are found in ruminant fat (eg, butter fat has 2-7%), where they arise from the action of microorganisms in the rumen, but the main source in the human diet is from partially hydrogenated vegetable oils (eg, margarine). Trans fatty acids compete with essential fatty acids and may exacerbate essential fatty acid deficiency. Moreover, they are strucmrally similar to samrated fatty acids (Chapter 14) and have comparable effects in the promotion of hypercholesterolemia and atherosclerosis (Chapter 26). [Pg.192]

Randle PJ The glucose-fatty acid cycle—biochemical aspects. Atherosclerosis Rev 1991 22 183-... [Pg.236]

MARCKMANN p, sandstrOm b, jespersen J (1990) Effect of total fat content and fatty acid composition in diet on factor Vll coagulant activity and blood lipids, Atherosclerosis, 80, 227-33. [Pg.296]

FIGURE 9. Endogenous lipoprotein metabolism. In liver cells, cholesterol and triglycerides are packaged into VLDL particles and exported into blood where VLDL is converted to IDL. Intermediate-density lipoprotein can be either cleared by hepatic LDL receptors or further metabolized to LDL. LDL can be cleared by hepatic LDL receptors or can enter the arterial wall, contributing to atherosclerosis. Acetyl CoA, acetyl coenzyme A Apo, apolipoprotein C, cholesterol CE, cholesterol ester FA, fatty acid HL, hepatic lipase HMG CoA, 3-hydroxy-3-methyglutaryl coenzyme A IDL, intermediate-density lipoprotein LCAT, lecithin-cholesterol acyltransferase LDL, low-density lipoprotein LPL, lipoprotein lipase VLDL, very low-density lipoprotein. [Pg.178]

Treating mice with 23 led to the inhibition of atherosclerotic progression, whereas macrophage-specific knockout of LXR exacerbates atherosclerosis [111]. In vivo activation of LXR leads to increased fatty acid synthesis, accumulation of TG and the development of hepatic steatosis [109]. Successful LXR agonists will show desirable HDL elevation without these side effects [112]. [Pg.187]

Auwerx, J., Schoonjans, K., Fruchart, J. C., and Staels, B. (1996). Transcriptional control of triglyceride metabolism Fibrates and fatty acids change the expression of the LPL and apo C-111 genes by activating the nuclear receptor PPAR. Atherosclerosis 124(Suppl.), S29-S37. [Pg.80]

The three fat fuels and their metabolism are involved directly or indirectly in diseases such as diabetes mellitus, syndrome X, obesity, atherosclerosis and coronary heart disease, which are discussed in other chapters in this book. This section considers the problems associated with high blood levels of ketone bodies and long-chain fatty acids. [Pg.146]

Nuts Atherosclerosis Increase in ratio of monosaturated/saturated fatty acids which causes a decrease in the plasma level of LDL-cholesterol... [Pg.359]

Figure 22.6 How various factors increase the risk of atherosclerosis, thrombosis and myocardial infarction. The diagram provides suggestions as to how various factors increase the risk of development of the trio of cardiovascular problems. The factors include an excessive intake of total fat, which increases activity of clotting factors, especially factor VIII an excessive intake of saturated or trans fatty acids that change the structure of the plasma membrane of cells, such as endothelial cells, which increases the risk of platelet aggregation or susceptibility of the membrane to injury excessive intake of salt - which increases blood pressure, as does smoking and low physical activity a high intake of fat or cholesterol or a low intake of antioxidants, vitamin 6 2 and folic acid, which can lead either to direct chemical damage (e.g. oxidation) to the structure of LDL or an increase in the serum level of LDL, which also increases the risk of chemical damage to LDL. A low intake of folate and vitamin B12 also decreases metabolism of homocysteine, so that the plasma concentration increases, which can damage the endothelial membrane due to formation of thiolactone. Figure 22.6 How various factors increase the risk of atherosclerosis, thrombosis and myocardial infarction. The diagram provides suggestions as to how various factors increase the risk of development of the trio of cardiovascular problems. The factors include an excessive intake of total fat, which increases activity of clotting factors, especially factor VIII an excessive intake of saturated or trans fatty acids that change the structure of the plasma membrane of cells, such as endothelial cells, which increases the risk of platelet aggregation or susceptibility of the membrane to injury excessive intake of salt - which increases blood pressure, as does smoking and low physical activity a high intake of fat or cholesterol or a low intake of antioxidants, vitamin 6 2 and folic acid, which can lead either to direct chemical damage (e.g. oxidation) to the structure of LDL or an increase in the serum level of LDL, which also increases the risk of chemical damage to LDL. A low intake of folate and vitamin B12 also decreases metabolism of homocysteine, so that the plasma concentration increases, which can damage the endothelial membrane due to formation of thiolactone.
Despite the fact that trans fatty acids are unsaturated, their contributions to atherosclerosis are similar to those of saturated fats. This similarity in physiologic action can be attributed to which of the following ... [Pg.50]

The answer is B. Saturated fatty acids and trans fatty acids are structurally similar their hydrocarbon tails are relatively linear. This allows them to pack tightly together in semi-crystalline arrays such as the membrane bilayer. Such arrays have similar biochemical properties in terms of melting temperature (fluidity). Although some of the other properties listed are also shared by saturated and trans fats, they are not thought to account for the tendency of these fats to contribute to atherosclerosis. [Pg.51]

C.D. Folmes, A.S. Clanachan, G.D. Lopaschuk, Fatty acid oxidation inhibitors in the management of chronic complications of atherosclerosis, Curr. Atheroscler. Rep. 7 (2005) 63-70. [Pg.128]

CN125 Vas Dias, F. W., M. J. Gibney, and T. G. Taylor. The effect of polyunsatu-rated fatty acids on the n-3 and n-6 series on platelet aggregation and platelet and aortic fatty acid composi-tion in rabbits. Atherosclerosis 1982 43(2-3) 245-257. [Pg.149]

Wang Y, Jones PJ, Ausman LM, Lichtenstein AH. Soy protein reduces triglyceride levels and triglyceride fatty acid fractional synthesis rate in hypercholesterolemic subjects. Atherosclerosis 173, 269-275, 2004. [Pg.394]

Balk, E.M., Lichtenstein, A.H., Chung, M., Kupelnick, B., Chew, P., Lau, J. (2006). Effects of omega-3 fatty acids on serum markers of cardiovascular disease risk a systematic review. Atherosclerosis, 189, 19-30. [Pg.70]

While many of the poorer people on earth starve to death the problems of atherosclerosis and obesity affect many in wealthier societies.2533-0 Tire fat content of foods is often blamed, and, as discussed in Boxes 21-B and 22-B, the quality of fatty acids in the diet is very important. However, like fatty acids, carbohydrates are also metabolized via acetyl-CoA and can readily be converted to both fatty acids and cholesterol.2534 Obesity is largely a problem of excessive total caloric intake. [Pg.1205]


See other pages where Atherosclerosis fatty acids is mentioned: [Pg.585]    [Pg.758]    [Pg.939]    [Pg.942]    [Pg.1160]    [Pg.111]    [Pg.118]    [Pg.205]    [Pg.219]    [Pg.13]    [Pg.42]    [Pg.105]    [Pg.211]    [Pg.56]    [Pg.244]    [Pg.248]    [Pg.356]    [Pg.518]    [Pg.319]    [Pg.86]    [Pg.317]    [Pg.38]    [Pg.217]    [Pg.899]    [Pg.614]   


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