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Biochem Pharmacol. 1997 Jul 1;54(1):215-8.
Effects of gemfibrozil and clofibric acid on the uptake of taurocholate by isolated rat hepatocytes.

Sabordo L, Sallustio BC.

Department of Clinical Pharmacology, The Queen Elizabeth Hospital, Woodville, South Australia.

Clinical use of fibrate hypolipidaemic agents has been associated with an increased incidence of hepatobiliary dysfunction including increased bile lithogenicity, gallstone formation, and cholestasis. The hepatic transport of bile acids plays an important role in bile formation and flow, and interference with the hepatocellular transport of bile acids may result in hepatobiliary dysfunction. The aim of this study was to investigate the effects of gemfibrozil and clofibric acid on the uptake of taurocholate by rat isolated hepatocytes. In control hepatocyte preparations (N = 5) at 37 degrees, the uptake of taurocholate was described by saturable Michaelis-Menten kinetics with a mean (+/-SD) Km of 44.1 +/- 10.2 microM and Vmax of 62.0 +/- 23.0 nmol/10(6) cells/min. In the presence of 200 microM clofibric acid, there was no significant change in the kinetics of taurocholate uptake. However, in the presence of 200 microM gemfibrozil there was a statistically significant (P < 0.05) decrease in the Vmax of taurocholate uptake (32.0 +/- 18.2 nmol/10(6) cells/min, N = 5) and no change (P > 0.05) in Km (48.5 +/- 29.5 microM, N = 5). Gemfibrozil behaved as a non-competitive inhibitor of taurocholate uptake, with a Ki of 144 microM, which is approximately 50 times higher than the unbound gemfibrozil concentrations achieved clinically in humans. Thus, gemfibrozil and clofibric acid did not appear to directly alter the hepatic uptake of taurocholate at clinically relevant concentrations.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9296370&dopt=Abstract




Am Heart J. 1997 Sep;134(3):565-71.
Gemfibrozil treatment of hypertriglyceridemia: improvement on fibrinolysis without change of insulin resistance.

Jeng JR, Jeng CY, Sheu WH, Lee MM, Huang SH, Shieh SM.

Department of Medicine, Tri-Service General Hospital, Taipei, Taiwan.

The fibrinolytic and metabolic changes associated with gemfibrozil treatment of hypertriglyceridemia were evaluated in 16 patients with type IV hyperlipidemia by criteria of triglyceride levels > 250 mg/dl and total cholesterol levels < 220 mg/dl. The plasma triglyceride level was significantly lower (323 +/- 71 vs 189 +/- 57 mg/dl; p = 0.000) and high-density lipoprotein cholesterol level significantly higher (33.5 +/- 4.6 vs 38.0 +/- 6.7 mg/dl; p = 0.005) after 3 to 4 months of gemfibrozil treatment. However, the glucose and insulin metabolism measured by oral glucose challenge and insulin suppression tests showed no significant changes after gemfibrozil therapy. In contrast, plasma plasminogen activator inhibitor-1 antigen (36.9 +/- 12.4 vs 27.3 +/- 11.4 ng/ml; p = 0.008) and activity (15.5 +/- 5.5 vs 11.8 +/- 3.0 IU/ml; p = 0.009) and tissue plasminogen activator antigen (13.2 +/- 4.0 vs 10.4 +/- 3.7 ng/ml; p = 0.007) were significantly depressed, and tissue plasimogen activator activity (0.57 +/- 0.31 vs 0.69 +/- 0.38 IU/ml; p = 0.015) was significantly elevated by gemfibrozil. The data indicate that lowering plasma triglyceride and raising high-density lipoprotein cholesterol levels by gemfibrozil treatment also improved the fibrinolytic system without changes of insulin resistance and glucose intolerance in patients with isolated hypertriglyceridemia.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9327717&dopt=Abstract




Metabolism. 1997 Nov;46(11):1299-304.
Postprandial hemorrheology and apolipoprotein B metabolism in patients with familial hypertriglyceridemia.

Otto C, Pschierer V, Soennichsen AC, Schwandt P, Richter WO.

Department of Medicine II, Klinikum Grosshadern, University of Munich, Germany.

Impaired postprandial lipoprotein metabolism has been found to be related to the extent of coronary artery disease. Moreover, since dyslipoproteinemias are associated with impaired hemorrheology, we investigated the effect of postprandial hypertriglyceridemia on hemorrheological parameters before and after triglyceride-lowering therapy. Triglyceride-rich lipoproteins (TRLs) separated by ultracentrifugation (d < 1.006 g/dL) and chylomicrons and chylomicron remnants (quantified by apolipoprotein [apo] B-48 determination) were determined after a fat load in 10 patients with familial hypertriglyceridemia before and after therapy with gemfibrozil (900 mg daily). Lipid and hemorrheological parameters (plasma and whole-blood viscosity [PV and BV], red cell aggregation [RCA], hematocrit, and fibrinogen) were determined at baseline and every hour up to 6 hours postprandially. Fasting total triglycerides and TRL triglycerides significantly decreased with gemfibrozil therapy (P < .01). Total triglycerides postprandially increased from 9.53 +/- 1.72 to 14.47 +/- 2.07 mmol/L (TRL triglycerides by 61%) before therapy (P < .05) and from 4.61 +/- 1.28 to 7.17 +/- 0.99 mmol/L (TRL triglycerides by 57%) after therapy (P < .05). The postprandial TRL apo B increase was reduced with gemfibrozil (from 11.6 +/- 2.8 to 20.7 +/- 5.0 mg/dL with therapy v 19.0 +/- 7.6 to 33.0 +/- 12.5 mg/dL before therapy, P < .05, respectively) with a proportionally greater increase in apo B-48 (119% and 169%, respectively) compared with apo B-100 (64% and 64%, respectively). Fasting RCA was improved with lipid-lowering therapy (P < .05), but PV, BV, RCA, and fibrinogen did not show any statistically significant postprandial changes either before or after lipid-lowering therapy. In summary, we did not find any statistically significant changes in hemorrheological parameters, despite a strong postprandial increase of triglycerides. In particular, these findings were independent of fasting triglyceride levels. We conclude that triglyceride-lowering therapy by gemfibrozil had no substantial beneficial effects with respect to hemorrheology in patients with familial hypertriglyceridemia.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9361689&dopt=Abstract












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