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Biochem Pharmacol. 1993 Oct 19;46(8):1515-8.
Gemfibrozil modifies acyl composition of liver microsomal phospholipids from guinea-pigs without promoting peroxisomal proliferation.

Vazquez M, Alegret M, Adzet T, Merlos M, Laguna JC.

Unidad de Farmacologia y Farmacognosia, Facultad de Farmacia, Universidad de Barcelona, Spain.

Treatment with gemfibrozil modifies acyl composition of hepatic microsomal phosphatidylcholine and phosphatidylethanolamine in guinea-pigs. Palmitic (16:0) and palmitoleic (16:1) fatty acids are increased, and stearic (18:0) and oleic (18:1) are decreased; further, while linoleic acid [18:2 (n-6)] is increased by gemfibrozil treatment, the other constituents of the n-6 fatty acids family, including arachidonic acid [20:4 (n-6)], are decreased. As gemfibrozil is a potent inhibitor of fatty acid elongation in vitro (Sanchez et al., FEBS Lett 300: 89-92, 1992), the inhibition of this enzyme system by gemfibrozil treatment could be responsible for the observed results in vivo. These changes in fatty acid composition are accompanied by a decrease in serum lipids and, more important, are independent of peroxisomal proliferation.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8240405&dopt=Abstract




Proc Natl Acad Sci U S A. 1983 Jan;80(2):324-8.
Physiological and x-ray studies of potential antisickling agents.

Abraham DJ, Perutz MF, Phillips SE.

Several aromatic compounds have been found to inhibit the gelling of sickle cell hemoglobin. We have tried to correlate the antigelling activity of such compounds with the stereo-chemistry of their binding sites in the hemoglobin molecule. This approach led to the discovery that two known antilipoproteinemia drugs, clofibrate and gemfibrozil, have antigelling activity. X-ray analysis showed that three pairs of molecules of clofibric acid, the active metabolite of clofibrate, bound to the walls of the internal cavity of deoxyhemoglobin A; only one pair bound to a quite different site, between helices A, E, and H of the alpha chains of carbon monoxide hemoglobin A. Unlike other antigelling agents, clofibric acid and related compounds decrease rather than increase the oxygen affinity of hemoglobin.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6572894&dopt=Abstract




Biomed Pharmacother. 1997;51(4):164-9.
Fibrinolytic response in subjects with hypertriglyceridemia and low HDL cholesterol.

Cimminiello C, Vigorelli P, Piliego T, Soncini M, Toschi V, Arpaia G, Perolini S, Bonfardeci C.

S Carlo Borr General Hospital, Milan, Italy.

The combination of hypertriglyceridemia and low high-density lipoprotein cholesterol (HDL-C) appears to be an excessively high risk factor for coronary artery disease (CAD). In the Helsinki study, both coronary events and mortality were decreased by gemfibrozil, especially in subjects with low HDL-C and high triglycerides (TG). On the other hand, it is known that high levels of TG can be associated with high levels of circulating plasminogen activator inhibitor (PAI), which is also a possible risk factor for CAD. The aim of the present study was to see: 1) whether the combination of low HDL-C and high TG is associated with a more impaired fibrinolytic response than in either isolated condition, and 2) whether gemfibrozil administration can improve fibrinolysis in patients with both high TG and low HDL-C. Twelve non-obese, non-diabetic subjects (eight men, four women; mean age 55 +/- 13 yrs) with low HDL-C (< 35 mg/dL men; < 45 mg/dL women) and high TG (mean 253.6 +/- 42.6 mg/dL) entered the study (Group A). Additionally fourteen comparable subjects with normal HDL-C were also investigated (Group B), plus 12 comparable subjects with isolated low HDL-C (Group C). Ten healthy people served as the control group. The following plasma fibrinolytic parameters were measured: tissue plasminogen activator antigen, PAI antigen and activity, euglobulin fibrinolytic activity (EFA) on fibrin plates, plasminogen and alpha-2-antiplasmin activities. All except the latter two values were also measured after venous occlusion (vo). In baseline conditions, patients in Groups A and B had higher EFA values before vo and higher PAI-1 antigen and alpha-2-antiplasmin levels after vo than those of controls or the subjects in Group C. The relationship between PAI antigen and PAI activity and TG was not confirmed in our population (n = 48). We also saw no interference due to HDL-C, while there was a significant relationship between EFA before vo and both TG and cholesterol. After gemfibrozil treatment (600 mg bid for 12 weeks), the lipid profiles of subjects with high TG and low HDL-C were significantly improved. There was also a slight reduction of PAI activity after vo, while the PAI-1 antigen had decreased significantly from baseline after vo (56.3 +/- 13 ng/mL before vo; 48.4 +/- 21 ng/mL after vo; P = 0.04). The higher risk of CAD in patients with low HDL-C and high TG might be in part related to impairment of fibrinolysis, which occurs in patients with isolated high TG. The close relationship existing between both TG and cholesterol levels and fibrinolytic activity confirm the key role of this latter process in the development of CAD.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9207984&dopt=Abstract












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