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Lovastatin cholesterol-lowering effects

Together with y-oryzanol, tocotrienols are responsible for the cholesterol-lowering effect of rice bran oil (250). Tocotrienol concentrates have been shown to have a hypocholesterolemic effect in animals and humans (251-257) possibly because of inhibition of hepatic 3-hydroxy-3-methyl-glutaryl-CoA reductase (HMG-CoA reductase) (251, 258, 259). The presence of a-tocopherol at concentrations >20% in tocotrienol concentrates was, however, found to attenuate the inhibitory elfect of tocotrienols on HMG-COA reductase, thereby weakening their cholesterollowering activities (254). Tocotrienols were especially found to synergize the cholesterol-lowering effect of lovastatin (254). In addition, tocotrienols have been shown to influence certain hemostatic parameters and to reduce the occurrence of chemical-induced tumors in the rat (253). [Pg.1700]

Pectin and oat bran can reduce the cholesterol-lowering effects of lovastatin. [Pg.1109]

Other than RIF and Taxol, many other commonly used clinical drugs have also been shown to activate PXR. These include peptide-mimetic HIV protease inhibitors [53], the cholesterol-lowering lovastatin and the anti-inflammatory dexamethasone [54]. A more comprehensive analysis of the effect of commonly used clinical drugs on PXR activation has recently been published by Sinz and colleagues [55]. [Pg.300]

The introduction of the fungal metabolite lovastatin (26-9) has led to a sizeable class of clinically effective cholesterol lowering drugs. These agents, known familiarly as the statins, block an enzyme, HMG-CoA reductase, that is involved in the synthesis of mevalonate, an early precursor of cholesterol. Extensive work has... [Pg.400]

An even more serious form of FH is the homozygous type. Here, no functional LDL receptors are produced. Plasma cholesterol levels can reach over 1,000 mg/dL. Clinical disease arises in the early teens, frequently followed by fatal Mis by age 20 (Goldstein and Brown, 1983). Since cholesterol-lowering drugs to date owe their effectiveness to stimulation of LDL receptors, they have not been very useful here. More drastic but hazardous methods of treatment are being attempted. These may include plasmapheresis of LDL with LDL antibodies and liver transplant that restored LDL receptors to about half normal levels, thereby permitting follow-up drug treatment with lovastatin to maintain normal cholesterol levels. [Pg.521]

In conclusion, uptake of Pu-Erh tea lowers plasma cholesterol and triacylglycerol in cholesterol-fed hamsters. The lipid lowering effects of Pu-Erh tea is likely caused by a combination of lovastatin and tea polyphenols. As a naturally fermented tea with lower EGCG and other catechins, Pu-Erh tea still exhibits strong antioxidant activities to scavenge DPPH radical and inhibit LDL oxidation in vitro and ex vivo. This study suggests that Pu-Erh tea drinking may reduce the risk factors in atherosclerosis-related ischemic heart disease. [Pg.101]

Over the last decade, several studies in tens of thousands of patients have revealed that lowering cholesterol, specifically lowering LDL cholesterol with statins, is effective for both primary and secondary prevention of IHD-related events. Statins shown to decrease morbidity and mortality associated with IHD include lovastatin, simvastatin, pravastatin, and atorvas-tatin.22,23 A recent meta-analysis showed that the risk of major adverse cardiac events is reduced by 21% with the use of statins in patients at high risk for IHD-related events.23... [Pg.74]

The answer is d, (Hardman, pp 934-935.) Chenodeoxycholic acid (chenodiol) and ursodiol have proved to he effective in some patients with cholesterol gallstones. Lovastatin lowers blood cholesterol levels but has no effect on gallstones. Methyl tertiary butyl ether and a new agent, monoctanoin, are infused directly into the common duct and will dissolve gallstones. [Pg.233]

It is considered the most effective drug for lowering levels of cholesterol, triglycerides, and very low-density lipoproteins in the plasma and for moderately increasing the number of high-density lipoproteins. It is used for treating hyperlipoproteinemia that cannot be corrected by a special diet or physical exertion. Synonyms of lovastatin are lovalip, meva-cor, mevinacor, and sivlor and those of mevastatin are CS-500 and ML-236 B. [Pg.274]

Endocrine effects Statins interfere with cholesterol synthesis and lower circulating cholesterol levels and, as such, might theoretically blunt adrenal or gonadal steroid hormone production. Small declines in total testosterone with no commensurate elevation in LH have been noted with the use of fluvastatin. Pravastatin showed inconsistent results with regard to possible effects on basal steroid hormone levels atorvastatin, lovastatin, rosuvastatin, and simvastatin did not reduce basal plasma cortisol concentration or basal plasma testosterone concentration or impair adrenal reserve. Appropriately evaluate patients who display clinical evidence of endocrine dysfunction. Exercise caution when administering HMG-CoA reductase inhibitors with drugs that affect steroid levels or activity, such as ketoconazole, spironolactone, and cimetidine. [Pg.619]


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See also in sourсe #XX -- [ Pg.4 , Pg.82 , Pg.83 , Pg.84 , Pg.88 , Pg.99 , Pg.100 , Pg.101 ]




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