Oleic acid absorption from micellar solutions and emulsions in the rat.
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Hypertension development in the spontaneously hypertensive rat (SHR) leads to vascular wall widening by smooth muscle cell proliferation. In these cells, triglycerides (TG) and cholesteryl esters (CE) can accumulate until they become foam cells. We administrated two oleic rich oils, virgin olive (VOO) and high oleic sunflower oils (HOSO), to Wistar-Kyoto rats (WKY) and SHR because these oils have been reported to reduce the risk for coronary heart disease in hypertensive patients and SHR. After 12 weeks of feeding, we analyzed the TG and CE composition and the lipolytic (lipoprotein lipase, LPL, and non-LPL) activity in aortas of these animals. HOSO increased the content of linoleic acid in CE and TG of aortas from both WKY and SHR as compared with animals fed VOO by proportionally decreasing the content of oleic acid. Conversely, VOO reduced the LPL and non-LPL lipolytic activities, hence limiting the free fatty acids available for the synthesis of TG and CE in the vascular wall.
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Oleic acid labeled with 14C, (14C-OA) or 131I (131I-OA) and 131I-labeled linoleic acid (131I-LOA) were administered intravenously to rats and tissue distribution studies completed at various time intervals from 5 to 60 min. Tissue distribution of 131-I-labeled oleic acid or linoleic acid was also studied in dogs at 5- and 30-min time intervals after intravenous administration of the tracer dose. There were distinct differences in the patterns of tissue distribution between 14C-OA, 131I-OA, and 131I-LOA. Radioactivity concentration in the myocardium was the highest at all time intervals in the rats given 131I-OA only. In dogs, the myocardial uptake of 131I-OA was significantly higher than the radioactivity in the blood or other tissues at 30 min after injection. The disappearance rates of 131I-OA and 131I-LOA were almost identical but myocardial concentration of 131I-LOA at 30 min after the dose in the dog was half that of 131I-OA whereas 131I-LOA liver concentration was higher than that of 131I-OA. Since the concentrations of our formulated 131I-OA in the blood and in the myocardium are both highest at the earlier intervals, it should be difficult to detect myocardial ischemia or infarction with 131I-OA scanning.
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The cholesteryl ester flow between high-density lipoproteins (HDL) and triglyceride-rich lipoproteins was investigated utilizing HDL fractions and synthetic lipid emulsion particles (EM). HDL was labeled in vitro with [1,2-3H(n)]cholesteryl ester or with [1,2,6,7-3H(n)]cholesteryl oleate, whereas EM were made with [4-14C]cholesteryl oleate (CO) or [carboxyl-14C]triolein (TO). The cholesteryl ester (CE) transfer rate between HDL and EM was spontaneous to some extent (because it occurred in saline medium), saturable, enhanced in a dose-dependent manner by the plasma fraction at D > 1.21 g/ml ascribed to its CETP activity, and greater for HDL3 than for HDL2. Unesterified fatty acids in the medium elicited two opposing effects: (1) enhanced the spontaneous cholesteryl oleate shift to EM and inhibited the reverse flow from EM to HDL3 but not to HDL2; (2) partially impaired the plasma D > 1.21 g/ml-induced bidirectional cholesteryl oleate flow. Approx. 2 mol TO from EM exchange for 1 mol CO from HDL3. Net cholesteryl ester balance was dependent on the concentration of HDL-cholesteryl ester, and independent from EM-cholesteryl oleate, possibly due to the much smaller concentration of the latter. These in vitro experiments shed light on the complex physical chemistry of transport of cholesteryl ester and triolein between HDL and TG-rich lipoproteins which occurs during the metabolism of chylomicrons in plasma.
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