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J Agric Food Chem. 1999 Nov;47(11):4731-5.
Effect of dietary lipid-lowering drugs upon plasma lipids and egg yolk cholesterol levels of laying hens.

Mori AV, Mendonca CX Jr, Santos CO.

Departamento de Clinica Medica, Faculdade de Medicina Veterinaria e Zootecnia, Universidade de Sao Paulo, Cidade Universitaria Armando de Salles Oliveira, Av. Orlando Marques de Paiva 87, Sao Paulo 05508-000, Brazil.

To evaluate the effect of lipid-lowering agents upon egg quality, reproductive performance, plasma lipids, and egg yolk cholesterol levels, 30-week-old Shaver laying hens were fed a basal diet (commercial ration) supplemented with 0.1% probucol (PROB), 0.025% gemfibrozil (GEMF), or lovastatin at 0.0005% (LOV1), 0.001% (LOV2), or 0.0015% (LOV3) for a 12-week experimental period. It was observed that the supplementation of the drugs did not impair albumen and shell quality. Hen performance was not adversely affected. The depression in triglyceride concentrations approached statistical significance only in LOV2 (38.5%), and total cholesterol was significantly depressed in LOV2 (36.0%), LOV3 (36.8%), PROB (29.6%), and GEMF (30.4%) treatments. Egg cholesterol content, expressed per gram of yolk, was significant lowered in LOV1 (7.5%) and LOV3 (12. 7%).

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10552881&dopt=Abstract




Comp Biochem Physiol B Biochem Mol Biol. 1999 Nov;124(3):289-94.
Effect of gemfibrozil on triacylglycerol synthesis and secretion by liver and lipoprotein lipase activity in adipose tissue of rats.

Nagao K, Sakono M, Nakayama M, Hirakawa T, Imaizumi K.

Department of Food Science and Technology, Faculty of Agriculture, Kyushu University, Fukuoka, Japan.

The role of gemfibrozil, a hypotriglyceridemic drug, in synthesis, secretion and catabolism of triacylglycerols (TG) in rats was assessed. Chow diet-fed Sprague-Dawley rats were given various doses of gemfibrozil (10, 30 and 100 mg/kg body weight) for 2 weeks. Rats receiving the drug at the lowest dose significantly lowered the concentration of serum TG and apolipoprotein (apo) B in comparison with control rats. Synthesis of fatty acids from [14C]acetate and esterification of [14C]oleate to TG by the liver were not suppressed by the drug. Secretion rates of TG and apo B, measured by the Triton method, were suppressed at the highest dose. Lipoprotein lipase activity of the acetone powder prepared from adipose tissue was not influenced by the drug. These results indicate that the primary cause of hypotriglyceridemic action of gemfibrozil is not due to suppressing synthesis and secretion of TG by the liver or enhancing lipoprotein lipase activity in adipose tissues.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10631806&dopt=Abstract




J Cardiovasc Pharmacol Ther. 1997 Jan;2(1):17-26.
Long-term Treatment With Pravastatin Alone and in Combination With Gemfibrozil in Familial Type IIB Hyperlipoproteinemia or Combined Hyperlipidemia.

Napoli C, Lepore S, Chiariello P, Condorelli M, Chiariello M.

Division of Cardiology, Federico II University of Naples, Naples, Italy

BACKGROUND: Pravastatin inhibits 3-hydroxy-3-methylglutaryl-coenzyme A reductase. It prevents mevalonate synthesis, reducing endogenous cholesterol production, and reduces cholesterol content in the liver, thus resulting in a down-regulation of low-density lipoprotein receptor production. Gemfibrozil reduces very low-density lipoprotein production and low-density lipoprotein-cholesterol level and increases very low-density lipoprotein catabolism. Therefore, it was suggested that combination therapy with both drugs could effect greater reduction of cholesterol levels as compared to pravastatin alone. The present study was carried out to evaluate the efficacy and safety of pravastatin as a monotherapy or in combination with gemfibrozil in the treatment of patients with familial type IIb hyperlipoproteinemia or familial combined hyperlipidemia. METHODS AND RESULTS: Forty-one patients were included in the study. All patients initially followed 6 weeks of hypolipidemic diet; subsequently they were randomized and received either 20 mg once daily of pravastatin alone (n = 13) or 20 mg of pravastatin together with 600 mg of gemfibrozil twice daily (n = 14). As a control, 14 patients were treated with diet only. The treatment lasted 24 months and clinical evaluation and laboratory tests were done at given time points. Both groups of treated patients showed an early reduction (3 months) of total (about 30% P <.01 vs controls), low-density lipoprotein (about 35%, P <.01 vs controls) and very low-density lipoprotein cholesterol levels (about 18%, P = NS). In contrast, high-density lipoprotein cholesterol levels increased significantly in patients treated with pravastatin and gemfibrozil (about 20%, P <.05 vs controls). Pravastatin treatment alone reduced the level of serum triglycerides as efficiently as in combination with gemfibrozil. Data showed a sustained normalization of lipid profile until 24 months. However, this effect was achieved in patients that had rather low levels of triglycerides. During the treatment we did not observe any difference in the incidence of possible drug-related side effects. Severe myopathy or rhabdomyolysis was not observed at the doses of the drugs used in our study. CONCLUSIONS: Therapy with pravastatin and in combination with gemfibrozil resulted in significant and sustained normalization of lipid profile in high-risk patients with familial type IIb hyperlipoproteinemia or familial combined hyperlipidemia.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10684438&dopt=Abstract [PubMed - as supplied by publisher]













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