Modulation of the effects of chylomicron remnants on endothelial function by minor dietary lipid components (original) (raw)
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The Journal of nutrition, 1995
Enrichment of lipoproteins with fatty acids derived from animal and/or plant fats may modify the oxidizability of lipoproteins and their effects on endothelial barrier function. To test this hypothesis, rabbits were fed for 30 days diets containing 2 g corn oil/100 g diet (low fat diet) or low fat supplemented with 16 g/100 g diet of corn oil, corn oil with added cholesterol, milk fat, chicken fat, beef tallow or lard. Compared with those fed the low fat, serum and LDL cholesterol concentrations were significantly lower in rabbits fed corn oil and greater in animals fed corn oil with added cholesterol or chicken fat. In contrast to the cholesterol data, lipid hydroperoxide levels were highest in oxidized LDL derived from rabbits fed corn oil or lard. LDL vitamin E levels were highest in rabbits fed corn oil with added cholesterol. The significant elevations in linoleic acid [18:2(n-6)] in serum and LDL may partially explain the high oxidizability of LDL in rabbits fed corn oil. LDL ...
Effects of flavonoids on the susceptibility of low-density lipoprotein to oxidative modification
Prostaglandins, Leukotrienes and Essential Fatty Acids, 2003
Antioxidant consumption has been reported to be inversely associated with the incidence of coronary artery disease. To clarify the possible role of vitamin E and volatile oils in the prevention of atherosclerosis, the effects of these compounds on the susceptibility of low-density lipoprotein (LDL) to oxidative modification were investigated. In this study, vitamin E and seven volatile oils "anethol, eugenol, geraniol, limonene, linalool, pulegone and thymol" were added to plasma and incubated at 37°C for 3 h. The LDL fraction was separated by ultracentrifugation and the oxidizability of LDL was estimated by measuring conjugated diene (CD), lipid peroxides and thiobarbituric acid-reactive substances (TBARS) after cupric sulfate solution was added. The data show that vitamin E, thymol and eugenol significantly and dose-dependently prolonged the lag time before initiation of oxidation reaction (P<0.01 by ANOVA). Also, vitamin E and thymol suppressed the formation of lipid peroxides and TBARS more markedly than other volatile oils. The ability to prolong lag time, suppression of lipid peroxides and TBARS formation was in the following order: vitamin E > thymol > eugenol > geraniol > linalool > limonene > anethol > pulegone. These data clearly show that LDL exposed to vitamin E and volatile oils in vitro reduces oxidizability; therefore have favorable effects in ameliorating atherosclerosis.
Endothelial cells as targets for chylomicron remnants
Atherosclerosis Supplements, 2010
Endothelial dysfunction is characterised by pro-inflammatory/pro-coagulant changes in the endothelium and supports leukocyte adhesion and transmigration, key steps in early atherogenesis. There is emerging evidence that triacylglycerol-rich lipoproteins (TGRLs) present in the circulation during the postprandial phase influence vascular inflammation but the specific contribution of the remnant lipoprotein component of TGRLs is largely unexplored and the mechanistic basis of their actions poorly defined. This article provides a brief overview of the evidence supporting direct actions of these particles on endothelial cells and highlights the importance of their fatty acid composition and oxidative state as determinants of their cellular actions.
The Journal of Nutrition, 2004
Minor components of virgin olive oil (VOO) may play a key role in the beneficial effects of VOO on atherosclerosis. In the present study we evaluated the influence of the unsaponifiable fraction of VOO on the production of eicosanoids and nitric oxide (NO) by endothelial cells (HUVECs). Triglyceride-rich lipoprotein (TRLs) were isolated from human serum after the intake of meals enriched in 3 high-oleic acid oils, i.e., high-oleic sunflower (HOSO), VOO, or enriched-virgin olive (EVO) oils, the last-mentioned containing 2.4% of unsaponifiable matter. HOSO induced a greater accumulation of triglycerides (TGs) in the postprandial serum than VOO or EVO, as measured by calculating the area under the curve. The incubation with TRLs increased NO release by endothelial cells compared with untreated control cells, but the effects of the various TRLs did not differ. EVO-derived TRLs reduced the production of prostaglandin E 2 (PGE 2) and thromboxane B 2 (TxB 2) (the stable metabolite of TxA 2) compared with VOO-or HOSO-derived TRLs. The release of PGI 2 (as 6-keto PGF 1␣) was similarly diminished by all TRLs compared with the control. In conclusion, the unsaponifiable fraction of VOO does not affect postprandial triglyceridemia, but it has favorable effects on endothelial function, mainly by reducing proinflammatory and vasoconstrictor eicosanoid synthesis (PGE 2 and TxB 2).
The British journal of nutrition, 1999
The Golden Syrian hamster (Mesocricetus auratus) has been shown to be a useful model of both human lipoprotein metabolism and the development of atherosclerosis. We report the effects of dietary lipids on the progression and regression of atherosclerosis in this model. In the first study, hamsters fed on coconut oil (150 g/kg diet) and cholesterol (30 g/kg diet) developed lipid-rich lesions in the ascending aorta (0.28 (SD 0.14) mm2) and aortic arch (0.01 (SD 0.01) mm2) after 4 weeks that continued to progress over the next 8 weeks (0.75 (SD 0.41) mm2 and 0.12 (SD 0.11) mm2 for the ascending aorta and aortic arch respectively). Removal of cholesterol from the diet halted this progression. Furthermore, in animals fed on olive oil in the absence of added cholesterol, plasma LDL-cholesterol concentrations were lower (P < 0.05) and the extent of atherosclerotic lesions was reduced (P < 0.001 for both regions of the aorta) compared with animals fed on coconut oil (with no added cho...
Atherosclerosis, 2004
Consumption of oily fish and fish oils is associated with protection against cardiovascular disease. Paradoxically, long-chain polyunsaturated fatty acids present in low-density lipoprotein (LDL) are suggested to be susceptible to oxidation. It is not clear whether eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) have similar effects on the susceptibility of LDL to oxidation or whether they affect the thrombogenicity of oxidized LDL. This study examined the influence of highly purified preparations of EPA and DHA on LDL oxidizability and LDL-supported thrombin generation in healthy human volunteers.
Atherosclerosis, 1998
A system for the perfusion of the isolated rat aorta which allowed the study of both the uptake of chylomicron remnants by the artery wall and their effects on endothelial function was developed. Perfusion for 2 h with 125 I-labelled native or oxidised (by treatment with copper sulphate) chylomicron remnants showed that small amounts became associated with the artery wall (0.1119 0.034 and 0.216 9 0.082 ng protein/mg tissue, respectively). Tests on endothelial function were carried out in vessel rings prepared after perfusion of the aortas in the presence or absence of chylomicron remnants for 2 h. After perfusion of the vessels with oxidised chylomicron remnants, the maximum response to phenylephrine (PE) was significantly increased (from 0.34 9 0.06 to 0.5190.04 g/mg tissue; PB0.05), while the maximum % relaxation to carbachol (CCh) was significantly decreased (from 91.6 9 2.4 to 71.5 9 7.2; PB 0.05) and the response to S-nitroso-N-acetylpenicillimine (SNAP) was unaffected. Perfusion with native chylomicron remnants showed a tendency to induce similar effects, although the changes observed did not reach statistical significance. As the lipoproteins were not present in the solution bathing the vessel rings during these tests, these effects can be attributed to perfusion of the aortas with chylomicron remnants, despite only small quantities being associated with the artery wall. The results suggest that oxidised chylomicron remnants influence vascular endothelial function by interfering with the L-arginine-nitric oxide (NO) pathway. The observed potentiation of contraction to PE may be due to inhibition of the basal release of NO or to the release of contractile factors. These findings support a role for dietary lipoproteins in the modulation of endothelial cell function which occurs in the pathogenesis of atherosclerosis.