Drugs online research references
Biochim Biophys Acta. 1993 Jan 10;1165(3):299-305.
An enzymatic explanation of the differential effects of oleate and gemfibrozil on cultured hepatocyte triacylglycerol and phosphatidylcholine biosynthesis and secretion.
Lamb RG, Koch JC, Bush SR.
Department of Pharmacology and Toxicology, Medical College of Virginia, Richmond 23298-0613.
Incubation (1-4 h) of primary cultures of adult rat hepatocytes with gemfibrozil (0.1-1.0 mM) significantly decreased the: (1) incorporation of [1,3-14C]glycerol into cellular triacylglycerol (30%); (2) secretion of labeled (VLDL) triacylglycerol (4-fold); and (3) oleate-induced rise in triacylglycerol biosynthesis and secretion. Gemfibrozil also increased the: (1) incorporation of labeled glycerol into cellular phosphatidylcholine (2-fold); and (2) secretion of labeled (HDL) phosphatidylcholine (10-fold). The gemfibrozil-dependent increase in the flux of labeled diacylglycerol into phosphatidylcholine is rapid (15 min) and associated with a 2-fold increase in membrane-bound phosphocholine cytidylyltransferase activity. A phosphocholine cytidylyltransferase-mediated rise in cellular CDP choline content may explain the gemfibrozil-dependent rise in phosphatidylcholine biosynthesis since homogenates of monolayers incubated with CDP choline preferentially incorporate labeled diacylglycerol into phosphatidylcholine rather than triacylglycerol. Therefore, the triacylglycerol-lowering potential of gemfibrozil may be due in part to its ability to shunt liver cell diacylglycerol into phosphatidylcholine rather than triacylglycerol. These results suggest that CDP choline may be a key regulator of the diacylglycerol branchpoint, since diacylglycerol is primarily incorporated into phosphatidylcholine or triacylglycerol depending on whether CDP choline is or is not available.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8418887&dopt=Abstract
Am J Prev Med. 1989 Mar-Apr;5(2):90-4.
Changes in pharmacologic treatment of hyperlipidemia.
Crouse JR 3rd, Ryu JE, Kahl FR.
department of Medicine, Wake Forest University Medical Center, North Carolina.
We evaluated the changes in frequency of pharmacologic treatment of hyperlipidemia in 345 hyperlipidemic patients with symptomatic cardiovascular disease requiring cardiac catheterization between 1982 and 1987. The frequency of pharmacologic treatment increased from 13% (1982) to 59% (1987), with the major increase occurring in 1984. Increases in the frequency of treatment were paralleled by increases in prescriptions for lipid-lowering drugs nationwide. During this period the percentage of hyperlipidemic patients we evaluated who were treated with various agents changed, and at the end of the study the use of gemfibrozil, bile acid-binding resins, and nicotinic acid had increased, whereas clofibrate and probucol use decreased. Although the data showed an increase in prevalence of treatment, almost half the patients remained untreated, and of those treated over half remained hypercholesterolemic despite treatment. The results suggest increasing but incomplete physician awareness of hyperlipidemia as a cardiovascular disease risk factor and the need for further physician education in the pharmacologic management of hyperlipidemia.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2730796&dopt=Abstract
Arch Intern Med. 1994 Jan 10;154(1):73-82.
Lipoprotein responses to treatment with lovastatin, gemfibrozil, and nicotinic acid in normolipidemic patients with hypoalphalipoproteinemia.
Vega GL, Grundy SM.
Center for Human Nutrition, University of Texas Southwestern Medical Center at Dallas.
BACKGROUND: The lipoprotein responses to conventional lipid-modifying drugs have not been adequately evaluated in normolipidemic patients with hypoalphalipoproteinemia (low levels of high-density lipoproteins). The purpose of this study was to compare responses to lovastatin, gemfibrozil, and nicotinic acid in such patients. METHODS: The first phase of the study compared lipoprotein responses to lovastatin and gemfibrozil in 61 middle-aged men with low levels of high-density lipoproteins. In the second phase, 37 patients agreed to take nicotinic acid; 27 patients finished this phase at a dose of 4.5 g/d. Nicotinic acid results were compared with those with lovastatin and gemfibrozil in the same patients. RESULTS: In the first phase, both drugs effectively lowered triglyceride levels. Gemfibrozil therapy increased high-density lipoprotein cholesterol levels by 10% and lovastatin by 6%, but lovastatin was much more effective for reducing low-density lipoprotein levels. Nicotinic acid did not significantly lower low-density lipoprotein levels in the second phase, but it raised high-density lipoprotein levels by 30%. CONCLUSIONS: Gemfibrozil therapy produced the least favorable response of the three drugs. Lovastatin markedly lowered low-density lipoprotein levels but only modestly raised levels of high-density lipoprotein, whereas nicotinic acid had the opposite effect. Consequently, the latter two drugs similarly reduced low-density lipoprotein-high-density lipoprotein ratios, although these effects were obtained in different ways. Between these two drugs, lovastatin therapy was more likely to reduce low-density lipoprotein cholesterol levels to below 2.6 mmol/L (100 mg/dL), and in view of recent recommendations, it may be preferable to nicotinic acid for many normolipidemic patients with established coronary heart disease.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8267492&dopt=Abstract
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