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Low-density lipoproteins cholesterol and

The a-blockers have favorable effects (decreased low-density lipoprotein cholesterol and increased high-density lipoprotein cholesterol levels). However, because they do not reduce CV risk as effectively as thiazide diuretics, this benefit is not clinically applicable. [Pg.140]

Vogelvang TE, Mijatovic V, Kenemans P, Teerlink T, van der Mooren MJ (2004) HMR 3339, a novel selective estrogen receptor modulator, reduces total cholesterol, low-density lipoprotein cholesterol, and homocysteine in healthy postmenopausal women. Fertil Steril 82 1540-1549... [Pg.246]

Friedman, M., Fitch, T. E., Levin, C. E., Yokoyama, W. Ft. (2000a). Feeding tomatoes to hamsters reduces their plasma low-density lipoprotein cholesterol and triglycerides. J. Food Set, 65, 897-900. [Pg.157]

Effects of crystalline nicotinic acid-induced hepatic dysfunction on serum low-density lipoprotein cholesterol and lecithin cholesteryl acyl transferase. Am J Cardiol 1998 81(6) 805-7. [Pg.564]

Clinical findings may include hypertrophied muscles, acne, oily skin, hirsutism in females, gynecomastia in males, and needle punctures. Edema and jaundice may develop in heavy users. Common laboratory abnormalities include elevated hemoglobin and hematocrit measurements, elevated low-density lipoprotein cholesterol and depressed high-density lipoprotein cholesterol levels. Liver function test results may be elevated, and luteinizing hormone levels are usually depressed. [Pg.738]

Ishikawa et al. (70), in a double-blind, cross-over trial in hypercholesterolemic patients, demonstrated that GLA lowered low-density lipoprotein cholesterol and apolipoprotein B in plasma and increased HDLC levels without affecting the levels of total cholesterol. Jantti et al. (71) observed a decrease in plasma... [Pg.1449]

Nicolosi, R.J., Ausman, L.M. and Hegsted, D.M. (1991) Rice bran oil lowers serum total and low-density lipoprotein cholesterol and apo B levels in non-human primates. Atherosclerosis, 88, 133-142. [Pg.325]

Fig. 1. Hazard ratios, with 95% confidence intervals as floating absolute risks, as estimate of association between category of update mean HbAlc concentration and any end point or deaths related to diabetes and all cause mortality. Reference category (hazard ratio 1.0) is HbAlc <6% with log-linear scales, p-value reflects contribution of glycaemia to multivariate model. Data adjusted for age at diagnosis of diabetes, sex, ethnic group, smoking, presence of albuminuria, systolic blood pressure, high- and low-density lipoprotein cholesterol and triglycerides [2]. Fig. 1. Hazard ratios, with 95% confidence intervals as floating absolute risks, as estimate of association between category of update mean HbAlc concentration and any end point or deaths related to diabetes and all cause mortality. Reference category (hazard ratio 1.0) is HbAlc <6% with log-linear scales, p-value reflects contribution of glycaemia to multivariate model. Data adjusted for age at diagnosis of diabetes, sex, ethnic group, smoking, presence of albuminuria, systolic blood pressure, high- and low-density lipoprotein cholesterol and triglycerides [2].
Health Benefits. Dietary capsaicin has been suggested to be useful for the prevention of cancer, e.g., human colon cancers based on experimental results obtained with male rats (Yoshitani et al. 2(X)1). Capsaicinoids increase the resistance of isolated LDL (low density lipoprotein) cholesterol and/or oils and fats to oxidation, when incubated together. This is caused by delaying the initiation and/or slowing the rate of oxidation. For the first time such effects have been checked on whole serum thus reflecting the in vivo situation more closely than isolated LDL. It has been shown that oxidation of serum lipids has been reduced also. A 50% increase of the lag time (time before initiation of oxidation) could be determined in a concentration of -0.6 jM capsaicin and dihydrocapsaicin. Furthermore, the rate of oxidation (slope of propagation phase) decreased with increasing concentrations of the capsaicinoids (Ahuja et al. 2006). [Pg.291]

Figure 25-4. Metabolic fate of very low density lipoproteins (VLDL) and production of low-density lipoproteins (LDL). (A, apolipoprotein A B-100, apolipoprotein B-100 , apolipoprotein C E, apolipoprotein E HDL, high-density lipoprotein TG, triacylglycerol IDL, intermediate-density lipoprotein C, cholesterol and cholesteryl ester P, phospholipid.) Only the predominant lipids are shown. It is possible that some IDL is also metabolized via the LRP. Figure 25-4. Metabolic fate of very low density lipoproteins (VLDL) and production of low-density lipoproteins (LDL). (A, apolipoprotein A B-100, apolipoprotein B-100 , apolipoprotein C E, apolipoprotein E HDL, high-density lipoprotein TG, triacylglycerol IDL, intermediate-density lipoprotein C, cholesterol and cholesteryl ester P, phospholipid.) Only the predominant lipids are shown. It is possible that some IDL is also metabolized via the LRP.
Figure 26-5. Factors affecting cholesterol balance at the cellular level. Reverse cholesterol transport may be initiated by pre 3 HDL binding to the ABC-1 transporter protein via apo A-l. Cholesterol is then moved out of the cell via the transporter, lipidating the HDL, and the larger particles then dissociate from the ABC-1 molecule. (C, cholesterol CE, cholesteryl ester PL, phospholipid ACAT, acyl-CoA cholesterol acyltransferase LCAT, lecithinicholesterol acyltransferase A-l, apolipoprotein A-l LDL, low-density lipoprotein VLDL, very low density lipoprotein.) LDL and HDL are not shown to scale. Figure 26-5. Factors affecting cholesterol balance at the cellular level. Reverse cholesterol transport may be initiated by pre 3 HDL binding to the ABC-1 transporter protein via apo A-l. Cholesterol is then moved out of the cell via the transporter, lipidating the HDL, and the larger particles then dissociate from the ABC-1 molecule. (C, cholesterol CE, cholesteryl ester PL, phospholipid ACAT, acyl-CoA cholesterol acyltransferase LCAT, lecithinicholesterol acyltransferase A-l, apolipoprotein A-l LDL, low-density lipoprotein VLDL, very low density lipoprotein.) LDL and HDL are not shown to scale.
To control risk factors and prevent major adverse cardiac events, statin therapy should be considered in all patients with ischemic heart disease, particularly in those with elevated low-density lipoprotein cholesterol. In the absence of contraindications, angiotensin-converting enzyme inhibitors should be considered in ischemic heart disease patients who also have diabetes melli-tus, left ventricular dysfunction, history of myocardial infarction, or any combination of these. Angiotensin receptor blockers... [Pg.63]


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See also in sourсe #XX -- [ Pg.237 ]




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