[Clearance of lipid emulsions used in parenteral feeding: study by perfusion of the isolated rat liver and in vivo exploration in the minipig].
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Biomedical subjects
Publications and source records attributed to J C Fruchart.
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Lipids, lipoproteins and apolipoproteins were analyzed in plasma of a city living Algerian population (Oran) free of obvious pathology. 129 individuals of this population were compared to a sample of subjects living in the surroundings of Lille (France). Several parameters were significantly different between the two populations. Cholesterol and phospholipids were lower in the population of Oran when compared with the population of Lille (4.90 mmol/l versus 5.47 mmol/l; 2.73 mmol/l versus 3.22 mmol/l respectively). Lipoproteins LpAI and LpAI:All were also lower in the population of Oran in comparison with the population of Lille (0.38 g/l versus 0.52 g/l; 0.68 g/l versus 1.00 g/l respectively), while LpCIII:B, LpE:B and Lp(a) were higher in the population of Oran when compared with the population of Lille (0.09 g/l versus 0.06 g/l; 0.28 g/l versus 0.16 g/l; 0.1 g/l versus 0.048 g/l) respectively. Several results argue in favor of the use of these lipoprotein parameters to better define the atherosclerotic risk. This was the main reason for characterizing the lipoprotein profile of such a population with a still unknown cardiovascular disease incidence.
INTRODUCTION: Production of endothelin by endothelial cells depends on protein-kinase C (PKC) stimulation which has been reported to be inhibited by alpha-tocopherol (alpha-Toch) but not by beta-tocopherol (beta-Toch). The goal of this study was to determine whether alpha-Toch and beta-Toch inhibit endothelin secretion by endothelial cells. METHODS: and results In a first set of experiments, cultured bovine aortic endothelial cells (BAEC) were incubated for 48h with 100 micromol/l alpha-Toch or vehicle (0.1% ethanol), then cells were stimulated for 4 h or 20 h with thrombin. After stimulating bovine aortic endothelial cells with thrombin for 4 h, alpha-Toch inhibited PKC activity by 63% and endothelin secretion by 44%, whereas after 20 h of incubation with thrombin, alpha-Toch decreased the peptide secretion by 51%. In a second set of experiments, BAEC were incubated with increased concentrations (from 0 to 100 micromol/l) of alpha-Toch or beta-Toch, PKC activity and endothelin secretion were measured after thrombin stimulation as previously reported. In these experiments, alpha-Toch strongly inhibited thrombin-induced PKC activity and endothelin secretion in a dose-dependent manner, whereas beta-Toch was more than 10-fold less active than alpha-Toch in inhibiting these stimulations. Tocopherols (alpha-Toch + beta-Toch) produced a proportional correlation on both PKC stimulation and endothelin secretion by inhibiting the effect of thrombin. CONCLUSION: These data suggest that alpha-Toch strongly inhibits thrombin-induced endothelin secretion in vitro at least partly through PKC inhibition.