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PubMed2000

Transport mechanisms for long-chain polyunsaturated fatty acids in the human placenta.

To understand the placental role in the processes responsible for the preferential accumulation of maternal long-chain polyunsaturated fatty acids (LCPUFAs) in the fetus, we investigated fatty acid uptake and metabolism in the human placenta. A preference for LCPUFAs over nonessential fatty acids has been observed in isolated human placental membranes as well as in BeWo cells, a human placental choriocarcinoma cell line. A placental plasma membrane fatty acid binding protein (p-FABP(pm)) with a molecular mass of approximately 40 kDa was identified. The purified p-FABP(pm) preferentially bound with essential fatty acids (EFAs) and LCPUFAs over nonessential fatty acids. Oleic acid was taken up least and docosahexaenoic acid (DHA) most by BeWo cells, whereas no such discrimination was observed in HepG2 liver cells. Studies on the distribution of radiolabeled fatty acids in the cellular lipids of BeWo cells showed that DHA is incorporated mainly into the triacylglycerol fraction, followed by the phospholipid fraction; the reverse is true for arachidonic acid (AA). The greater cellular uptake of DHA and its preferential incorporation into the triacylglycerol fraction suggests that both uptake and transport modes of DHA by the placenta to the fetus are different from those of AA. p-FABP(pm) antiserum preferentially decreased the uptake of LCPUFAs and EFAs by BeWo cells compared with preimmune serum. Together, these results show the preferential uptake of LCPUFAs by the placenta that is most probably mediated via the p-FABP(pm).

Adult↗
PubMed1975

Incorporation of the dietary trans fatty acid (C18:1) into the serum lipids, the serum lipoproteins and adipose tissue.

Two diets, identical except for differences in trans and cis fatty acids, were fed to rabbits in order to evaluate the effects of dietary trans fatty acids on the fatty acid composition of serum lipids, lipoproteins and adipose tissue. The animals were first starved to deplete adipose tissue stores and then were red a diet containing 15% of the calories as C18:1 trans fatty acid (elaidic acid). A second group received a diet containing an equivalent amount of C18:1 cis fatty acid (oleic acid). A third group of animals, the control group, was fed only the baseline low fat rabbit chow. Dietary trans fatty acid was incorporated into all serum lipid and lipoprotein fractions and into the adipose tissue. In the serum the triglycerides contained the greatest amount of trans fatty acid followed by the phospholipids with cholesterol esters containing the least. The trans fatty acids of the phospholipids and cholesterol esters were distributed equally among the lipoprotein fractions, but the triglycerides of high density lipoproteins contained less trans fatty acids than did the triglycerides of other lipoproteins. Adipose tissue developed a high content of C18:1 trans fatty acid (21.7%), apparently at the expense of C18:1 cis fatty acid. In addition to the incorporation of C18:1 trans fatty acid, the content of other fatty acids, including C18:2 and the total of C18:1 cis and trans, was influenced by the substitution of dietary trans for cis fatty acids. The serum phospholipids of the trans-fed rabbits contained more C18:2 than the phospholipids of the cis-fed rabbits. The serum cholesterol esters of the trans-fed rabbits contained more C18:2 and a smaller total of C18:1 (cis puls trans) than the cholesterol esters of the cis-fed rabbits. These differences indicated that C18:1 trans fatty acid was not necessarily the metabolic equivalent of 18:1 cis fatty acid. These results suggested that dietary trans fatty acids which are contained in hydrogenated margarines, shortenings and oils of the human diet are readily incorporated into the lipids of the body including membranous structures such as lipoproteins.

Adipose Tissue↗
PubMed2002

Lovastatin does not accentuate but is rather additive to palmitate-induced apoptosis in cardiomyocytes.

Fatty acids such as palmitate have been observed to induce apoptosis in cardiomyocytes but the mechanism of this cytotoxicity is unresolved. The present study sought to determine whether an aspect of fatty acid metabolism is responsible for palmitate-induced apoptosis in cardiomyocytes. As palmitate metabolism increases acetyl CoA production via increased beta oxidation within the mitochondria, we hypothesized that increased acetyl CoA entering the cholesterol biosynthesis pathway might produce intermediates or end products that would be toxic to the cell. To test this hypothesis, cardiomyocytes from embryonic chick cardiomyocytes were treated with the 3-hydroxy-3-methylgutaryl CoA (HMG-CoA) reductase inhibitor lovastatin that inhibits the cholesterol biosynthesis pathway downstream of the acetyl CoA trimerization into HMG-CoA. Lovastatin did not inhibit palmitate-induced apoptosis. Rather, lovastatin induced significant apoptosis itself and when combined with palmitate, the level of apoptosis was equal to the sum of palmitate alone and lovastatin alone. This observation suggests that palmitate and lovastatin are inducing apoptosis by two independent mechanisms. A role for mitochondrial metabolism via carnitine palmitoyl transferase (CPT) in palmitate-induced apoptosis was suggested since capric acid, a fatty acid that is metabolized within the mitochondria but does not utilize CPT-1, did not induce apoptosis. Palmitate-induced apoptosis was further related to the metabolism of saturated fatty acids as the unsaturated fatty acid oleic acid did not induce apoptosis. These data suggest that a unique feature about palmitate metabolism independent of its role in cholesterol biosynthesis is responsible for palmitate-induced apoptosis and the effects of palmitate are additive to those of lovastatin to induce cardiac apoptosis.

Acridine Orange↗
PubMed1997

Cytotoxicity and apoptosis produced by arachidonic acid in Hep G2 cells overexpressing human cytochrome P4502E1.

The goal of the current study was to evaluate the effects of arachidonic acid, as a representative polyunsaturated fatty acid, on the viability of a Hep G2 cell line, which has been transduced to express human cytochrome P4502E1 (CYP2E1). Arachidonic acid produced a concentration- and time-dependent toxicity to Hep G2-MV2E1-9 cells, which express CYP2E1, but little or no toxicity was found with control Hep G2-MV-5 cells, which were infected with retrovirus lacking human CYP2E1 cDNA. In contrast to arachidonic acid, oleic acid was not toxic to the Hep G2-MV2E1-9 cells. The cytotoxicity of arachidonic acid appeared to involve a lipid peroxidation type of mechanism since toxicity was enhanced after depletion of cellular glutathione; formation of malondialdehyde and 4-hydroxy-2-nonenal was markedly elevated in the cells expressing CYP2E1, and toxicity was prevented by antioxidants such as alpha-tocopherol phosphate, 6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid (trolox), propylgallate, ascorbate, and diphenylphenylenediamine, and the iron chelator desferrioxamine. Transfection of the Hep G2-MV2E1-9 cells with plasmid containing CYP2E1 in the sense orientation enhanced the arachidonic acid toxicity, whereas transfection with plasmid containing CYP2E1 in the antisense orientation decreased toxicity. The CYP2E1-dependent arachidonic acid toxicity appeared to involve apoptosis, as demonstrated by terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling and DNA laddering experiments. Trolox, which prevented toxicity of arachidonic acid, also prevented the apoptosis. Transfection with a plasmid containing bcl-2 resulted in complete protection against the CYP2E1-dependent arachidonic acid toxicity. It is proposed that elevated production of reactive oxygen intermediates by cells expressing CYP2E1 can cause lipid peroxidation, which subsequently promotes apoptosis and cell toxicity when the cells are enriched with polyunsaturated fatty acids such as arachidonic acid. The Hep G2-MV2E1-9 cells appear to be a valuable model to study interaction between CYP2E1, polyunsaturated fatty acids, reactive radicals, and the consequence of these interactions on cell viability and to reproduce several of the key features associated with ethanol hepatotoxicity in the intragastric infusion model of ethanol treatment.

Antioxidants↗
PubMed2000

[GC-MS analysis of volatile componments in root of Ficus hitra].

The volatile components in root of Ficus hitra Vahl were analyzed by GC-MS, the results suggested that the main volatile components in root of Ficus hitra Vahl were Hexadecanoic acid, Oleic acid, Linolic acid and Ethyl Acetate; its ether extract contains Isopsoralen and Bergapten. Coumarins should be one of the effective sections in root of Ficus hitra Vahl.

Coumarins↗
PubMed1998

Activation of protein kinase C in human hepatocellular carcinoma (HEP3B) cells increases erythropoietin production.

Some investigators have reported previously that phorbol esters inhibit in vitro erythropoietin production stimulated by hypoxia; whereas others have reported that phorbol esters enhanced Epo production during exposure to hypoxia. We have demonstrated in the present experiments that hypoxia significantly increased diacylglycerol levels in cultured human hepatocellular carcinoma (Hep3B) cells. 1-oleoyl-2-acetyl-ras-glycerol (OAG) and N-(6-phenylhexyl)-5-chloro-1-naphthalenesulfonamide (SC-9), two well-known protein kinase C activators, significantly increased medium levels of erythropoietin as well as erythropoietin messenger RNA levels in normoxic Hep3B cells. A potent protein kinase C inhibitor, chelerythrine chloride, significantly decreased hypoxia-induced increases in medium levels of erythropoietin as well as erythropoietin messenger RNA levels in Hep3B cells. A cis-unsaturated free fatty acid, oleic acid, significantly enhanced OAG-induced medium levels of erythropoietin in normoxic Hep3B cells, whereas a phospholipase A2 inhibitor, mepacrine, significantly decreased hypoxia-induced erythropoietin production in Hep3B cells. These results provide strong support for a positive role for protein kinase C in the hypoxic regulation of erythropoietin production.

Alkaloids↗
PubMed1992

A high-performance liquid chromatography-based radiometric assay for acyl-CoA:alcohol transacylase from jojoba.

Acyl-CoA:alcohol transacylase catalyzes the final step in the biosynthesis of storage liquid wax esters from acyl-CoA fatty acids and fatty alcohols in a limited number of microbes, algae, and Simmondsia chinensis Link (jojoba). An improved and automated method of enzyme assay for this catalyst from cotyledons of jojoba is described. The assay method uses reversed-phase C18 high performance liquid chromatography (HPLC) to separate the labeled C30:1 liquid wax product, [14C]-dodecanyl-octadecenoate, from the unreacted substrate, [14C]octadecenoyl-CoA (oleyl-CoA), and other components produced from enzymes present in the crude homogenate of jojoba cotyledons, including [14C]-octadecenoic acid (oleic acid) and [14C]octadecenol (oleyol). Methods are also described for microscale chemical synthesis in one vessel of 14C-radiolabeled substrates and products for the transacylase. These labeled reagents are required to confirm the HPLC separations of reaction products. The radioactive components are quantitated using an on-line flow-through scintillation detector enabling sensitive and precise analysis of the reaction products.

Acyl Coenzyme A↗
PubMed1992

Oral delivery of a renin inhibitor compound using emulsion formulations.

The oral delivery of O-(N-morpholino-carbonyl-3-L-phenylaspartyl-L- leucinamide of (2S,3R,4S)-2-amino-1-cyclohexyl-3,4-dihydroxy-6-methylhetane (I), a new renin inhibitor, was studied in the in vivo rat model using emulsion formulations. The components of the emulsion formulations were chosen based on their proposed effects on membrane structure, membrane fluidity, and solute transport. The percent absolute bioavailability (%AB) of I was increased from 0.3% (water suspension) to 5.1% when long-chain unsaturated fatty acid (oleic acid, linoleic acid, etc.)- and mono- and diglyceride (monolein, dilaurin, etc.)-containing emulsion formulations were used. Considering very high first-pass liver extraction of the compound (80%), it is suggested that emulsion formulations increased the intestinal transport of the compound significantly. The solubility of I in aqueous media with and without bile salt (20 mM) was found to be low (approximately 1 micrograms/ml). Incubation in 0.01 N HCl did not affect the particle size of the emulsion. The titration of oleic acid/monoolein emulsion in a pH 6.5 medium with a mixed bile salt system indicated reduction in the particle size of the emulsion. Drug precipitation was observed above 30 mM bile salt concentrations. No drug crystals could be detected in the intestinal contents of the rats when emulsion formulations were ingested. These results suggest that in the intestine of the animals, the particle size of the emulsions is reduced in the presence of bile fluid while the drug resides primarily in the oil phase. The mechanism of enhanced transport of I from the emulsion formulations is discussed along with the possibility of cotransport for the drug and oil. Emulsion formulations can be a potential delivery form for low-bioavailable lipid-soluble drugs.

Absorption↗
PubMed1989

Saturation of fat and cholecystokinin release: implications for pancreatic carcinogenesis.

In a study to determine the effect of saturation of fats on their ability to stimulate cholecystokinin (CCK) release six normal volunteers ate five test meals containing different fats with intervals of 1 week. Plasma CCK levels were measured by a specific radioimmunoassay and the gallbladder volume was calculated from ultrasound measurements. The sodium salt of the monounsaturated fatty acid oleic acid (3.5 g) produced a significantly greater integrated CCK response than that of the saturated fatty acid stearic acid (mean [SEM] 103 [41] vs 8[41] pmol.l-1.min). The gallbladder contracted to 42 (3)% of its initial volume after oleate but remained at 89 (8)% of its initial volume after stearate. Integrated CCK responses to dietary triglycerides (30 g) also differed significantly according to the degree of saturation--277 (58) pmol.l-1.min after corn oil (predominantly diunsaturated), 143 (14) pmol.l-1.min after olive oil (predominantly monounsaturated), and 44 (12) pmol.l-1.min after suet (predominantly saturated). The finding that unsaturated fats are stronger stimulants of CCK release than saturated fats may explain the promotion of pancreatic carcinogenesis in rats by unsaturated but not saturated fats and may support the role of CCK in this effect.

Adult↗
PubMed2002

Edible arabinoxylan-based films. 1. Effects of lipid type on water vapor permeability, film structure, and other physical characteristics.

Arabinoxylans (AX) are natural fibers extracted from maize bran, an industrial byproduct. To promote this polymer as a food ingredient, development of edible coatings and films had been proposed. Indeed, composite arabinoxylan-based films were prepared by emulsifying a fat: palmitic acid, oleic acid, triolein, or a hydrogenated palm oil (OK35). Lipid effects on water vapor permeability (WVP), surface hydrophobicity (contact angles), lipid particle size, and mechanical properties were investigated. Results showed that OK35-AX emulsion films had the lowest WVP. Emulsified films presented a bimodal particle size distribution; however, the smallest particle mean diameter (0.54 microm) was observed in OK35-AX emulsion films. Contact angles of water comparable to those observed for LDPE films (>90 degrees ) are measured on the OK35-AX film surface. Finally, only triolein-AX emulsion films had elongation higher than films without lipid. These results suggest that OK35 enhances functional properties of AX-based films and should be retained for further research.

Chemical Phenomena↗
PubMed2001

A human cellular model for studying the regulation of glucagon-like peptide-1 secretion.

GLP-1 (glucagon-like peptide-1) is a potent insulin secretagogue released from L cells in the intestine. The regulation of GLP-1 secretion has been described both in vivo and in vitro in several animal species, but data from human cellular models are lacking. For this purpose, factors and cell-signaling pathways regulating GLP-1 secretion were investigated in the NCI-H716 human intestinal cell line. After differentiation, these cells homogeneously produced 16.8 pmol GLP-1/mg protein with a basal release of 4.2% during a 2-h incubation period. Nutrients, such as palmitic acid, oleic acid, and meat hydrolysate, stimulated GLP-1 secretion in a dose-dependent manner, as did the cholinergic agonist carbachol and the neuromediator gastrin-releasing peptide. Along with stimulating GLP-1 release, gastrin-releasing peptide, like ionomycin, increased intracellular calcium levels. Activators of PKA and PKC were able to increase GLP-1 secretion in NCI-H716 cells. However, neither PKA activators nor meat hydrolysate increased proglucagon mRNA levels. These findings indicate that the NCI-H716 cell line constitutes a unique model to study the cellular mechanism of GLP-1 secretion in humans and suggest potential interspecies divergence in the regulation of proglucagon gene expression in enteroendocrine cells.

Animals↗
PubMed1980

Triacylglycerol metabolism and triacylglycerol lipase activities of cultured human skin fibroblasts.

The relative contribution of lipoproteins and free fatty acid to the cellular triacylglycerol content of cultured human fibroblasts was tested. Fibroblasts accumulated triacylglycerol in proportion to the molar ratio of free fatty acid (oleic acid) to albumin in the medium. Fibroblasts also accumulated triacylglycerol when exposed to medium containing human very low density liproprotein. This accumulation of triacylglycerol was apparently due to direct uptake of intact very low density lipoprotein particles initiated by binding of very low density lipoprotein to cell surface receptors. The amount of 125I-labeled very low density lipoprotein protein internalized and degraded by the cell saturated at the same very low density lipoprotein concentration that produced the maximum increase in cell triacylglycerol. Preincubations with lipoprotein-deficient serum, which enhanced the cell's ability to bind 125I-labeled very low density lipoprotein, increased the amount of 125I-labeled very low density lipoprotein internalized and degraded by the cell in parallel with increased levels of cellular triacylglycerol. Results suggest that the triacylglycerol that accumulates in the presence of very low density lipoprotein represents a lysosomal pool of partially degraded very low density lipoprotein. Measurements of lipase activity of fibroblast homogenates revealed three pH optima at (in descending order of magnitude of activity) pH 4, pH 6, and pH 8. The pH 8 lipase does not appear to represent lipoprotein lipase, since it is not activated by either serum or heparin. Exposure of the cells to medium with varying lipid composition had no effect on the lipase activities. The lipase activities of fibroblasts from donors with familial hypertriglyceridemia appear to be normal.

Adult↗
PubMed2005

Differential utilization of saturated palmitate and unsaturated oleate: evidence from cultured myotubes.

We recently described a primarily reduced palmitate oxidation in myotubes established from type 2 diabetic subjects, whereas triacylglycerol (TAG) accumulation seemed to be adaptive. However, it is still uncertain whether these changes are similar for saturated and unsaturated fatty acids and whether high concentrations of glucose and/or insulin may change this picture. Studies of palmitic acid and oleic acid metabolism in human myotubes established from control and type 2 diabetic subjects under conditions of acute high concentrations of insulin and/or glucose may solve these questions. Total oleic acid and palmitic acid uptake in myotubes was increased during acute insulin stimulation (P < 0.01) but not under acute, high-glucose concentrations, and no differences were found between the groups. Type 2 diabetic myotubes expressed a reduced palmitic acid oxidation to carbon dioxide (P </= 0.04), whereas oleic acid oxidation showed no differences between myotubes from both groups. High glucose concentrations decreased oleic acid oxidation (P </= 0.03). Lipid distribution was not different in diabetic and control myotubes when palmitic acid and oleic acid incorporation into cellular lipids was compared. Myotubes that were exposed to palmitic acid showed an increased palmitic acid incorporation into diacylglycerol (DAG) and TAG compared with myotubes that were exposed to oleic acid (P < 0.05) expressing an increased intracellular free fatty acid (FFA) level (P < 0.05). Lipid distribution was not affected by high glucose, whereas insulin increased FFAs, DAG, and TAG (P < 0.05). De novo lipid synthesis from glucose in both diabetic and control myotubes was of the same magnitude independent of glucose and insulin concentrations. These results indicate that palmitic acid and oleic acid are utilized in the same pattern in diabetic and control myotubes even though palmitic acid oxidation is primarily reduced in diabetic cells. Palmitic acid and oleic acid are handled differently by myotubes: Palmitic acid seems to accumulate as DAG and TAG, whereas oleic acid accumulates as intracellular FFAs. These observations indicate that oleic acid is preferable as fatty acid as it accumulates to a lesser extent as DAG and TAG than palmitic acid. Neither acute hyperglycemia nor de novo lipid synthesis from glucose seems central to the TAG accumulation in obesity or type 2 diabetes.

Diabetes Mellitus, Type 2↗
PubMed1990

Role of leukotrienes during oleic acid-induced lung injury in pigs.

We hypothesized that leukotrienes might contribute to the pathophysiology of acute lung injury induced by oleic acid. Oleic acid (2-20 mg.kg-1.h-1), LY171883 [leukotriene (LT) D4/LTE4 receptor antagonist, 10 mg/kg + 1 mg.kg-1.h-1] + oleic acid (10 mg.kg-1. h-1), or triolein (20 mg.kg-1.h-1) were infused intravenously into anesthetized pigs. Treatment with the cyclooxygenase inhibitor was designed to possibly enhance LT release. Bronchoalveolar lavage fluid concentrations of LTB4, LTC4, LTD4, and LTE4 were measured by reverse-phase high-performance liquid chromatography and radioimmunoassay. Oleic acid caused dose-related hypoxemia and pulmonary hypertension and increased pulmonary vascular resistance, lung water, and alveolar-capillary membrane permeability. Bronchoalveolar lavage fluid levels of LTB4, LTC4, LTD4, and LTE4 showed no significant changes in oleic acid- or indomethacin + oleic acid-treated pigs, compared with triolein-treated controls. Indomethacin modestly attenuated the oleic acid-induced hypoxemia and the early increases (i.e., 0-0.5 h) in mean pulmonary arterial pressure and pulmonary vascular resistance. In contrast, LY171883 provided no protection against any oleic acid-induced cardiopulmonary effect (measured or calculated). We conclude that LTs are not likely to be important mediators of oleic acid-induced lung injury in the pig.

Acetophenones↗
PubMed1989

cis-unsaturated fatty acids stimulate catecholamine secretion, tyrosine hydroxylase and protein kinase C in adrenal medullary cells.

In digitonin-permeabilized bovine adrenal medullary cells, arachidonic acid and oleic acid, the cis-unsaturated fatty acids, enhanced Ca2+-induced secretion of catecholamines, whereas elaidic acid, a trans-unsaturated fatty acid and stearic acid, a saturated fatty acid, had no effect. Indomethacin, an inhibitor of cyclooxygenase and nordihydroguaiaretic acid, an inhibitor of lipoxygenase, failed to inhibit the stimulatory effect of arachidonic acid. Stimulation of catecholamine secretion by arachidonic acid was abolished by the removal of adenosine 5'-triphosphate and Mg2+ from the incubation medium. Pretreatment of the cells with phorbol 12-myristate 13-acetate, an activator of protein kinase C, enhanced Ca2+-induced catecholamine secretion. In cells pretreated with phorbol 12-myristate 13-acetate, the stimulatory effect of arachidonic acid on Ca2+-induced catecholamine secretion was greatly reduced. In digitonin-permeabilized cells, arachidonic acid and oleic acid enhanced Ca2+-induced activation of tyrosine hydroxylase in the presence of adenosine 5'-triphosphate and Mg2+, whereas elaidic acid and stearic acid did not activate the enzyme. In a soluble fraction of adrenal medullary cells, 32P incorporation to histone by protein kinase C was increased by arachidonic acid and oleic acid, but not by elaidic acid and stearic acid. These results suggest that cis-unsaturated fatty acids modulate Ca2+-induced catecholamine secretion and tyrosine hydroxylase activity by activation of protein kinase C in adrenal medullary cells.

Adenosine Triphosphate↗
PubMed1994

Evidence for a novel keratinocyte fatty acid uptake mechanism with preference for linoleic acid: comparison of oleic and linoleic acid uptake by cultured human keratinocytes, fibroblasts and a human hepatoma cell line.

Keratinocytes require the essential fatty acid (FA), linoleic acid (LA), for the synthesis of stratum corneum membrane lipids. A plasma membrane-FA binding protein (PM-FABP), is postulated to mediate cellular FA-uptake in hepatocytes and several other tissues, but the mechanism whereby exogenous FA are taken up by keratinocytes has not been investigated. This study examines the uptake of LA and oleic acid (non-essential) in cultured human keratinocytes, in comparison to dermal fibroblasts and the human hepatoma cell line, HepG2. As previously reported for hepatocytes, FA-uptake in keratinocytes was curvilinear, with an initial (30 s) rapid cellular influx. The initial uptake component was temperature dependent, exhibited saturable kinetics and was significantly inhibited by pretreatment with trypsin. In contrast, fibroblast FA-uptake lacked an initial rapid uptake component, was relatively temperature insensitive, and was not inhibited by trypsin. Keratinocytes differed from both hepatocytes and fibroblasts by more rapid uptake of LA in comparison to oleic acid during the initial influx phase. Moreover, FA-uptake in keratinocytes was not inhibited by preincubation with a anti-rat liver PM-FABP antibody. These data provide evidence for a PM-FA transporter in keratinocytes that is distinct from the hepatic PM-FABP. The apparent preference of the putative keratinocyte FA transporter for LA may function to ensure epidermal capture of sufficient LA for barrier lipid synthesis.

Adult↗
PubMed2003

Platelet aggregation, thromboxane production and thrombogenic ratio in postmenopausal women consuming high oleic acid-sunflower oil or palmolein.

BACKGROUND: Saturated fatty acids exert controversial effects on platelet aggregation and eicosanoid production. AIM: To investigate the effect of a dietary exchange between palmitic acid and oleic acid on both platelet aggregation and thromboxane B2 (TXB(2)) production, and on urine TXB(2), prostacyclin I2 (PGI(2) as 6-keto-protaglandin F(1)alpha), and the thrombogenic ratio (TXB(2)/6-keto-protaglandin F(1)alpha) in fourteen postmenopausal women. EXPERIMENTAL DESIGN: Women were assigned to two consecutive 28-d dietary periods that were high in cholesterol (~400 mg/d) and fat (~46%en). In the first period all subjects followed an oleic acid-rich diet prepared with high oleic acidsunflower oil. This was followed by a second period rich in palmitic acid in the form of palmolein. DETERMINATIONS: Nutrient intakes, ADP-platelet aggregation, platelet TXB(2) production, urine TXB(2) and 6-keto-protaglandin F(1)alpha were measured during two dietary periods and the results obtained correlated to serum cholesterol, lipoproteincholesterol and peroxides, apolipoproteins and plasma tocopherol. RESULTS: The palmolein diet led to an increase in the platelet aggregation rate (p < 0.05) and in the time for the maximal aggregation rate (p < 0.02). No significant differences were observed in platelet TXB(2) production. Palmolein increased urine TXB(2) in pg/mL (p < 0.05) and pg/min (p < 0.01), whereas the thrombogenic ratio (TXB(2)/6-keto-protaglandin F(1)alpha) did not change. Most changes were related to oil change, few to serum cholesterol level (< or > or = 6.2 mmol/L) or age (< or > or = 65 yr). CONCLUSIONS: Palmolein diet activates platelet aggregation more in normocholesterolemics. Though palmolein increased thromboxane and tended to increase prostacyclin in urine in normo- and hypercholesterolemic women, the thrombogenic ratio did not change. These effects were related to the LDL and HDL concentration increases and to the absence of change in the total cholesterol/HDL-cholesterol ratio found following the dietary intervention.

Aged↗
PubMed2000

Determination of the fatty acid composition of saponified vegetable oils using matrix-assisted laser desorption/ionization time-of-flight mass spectrometry.

A method using matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOFMS) for the determination of the fatty acid composition of vegetable oils is described and illustrated with the analysis of palm kernel oil, palm oil, olive oil, canola oil, soybean oil, vernonia oil, and castor oil. Solutions of the saponified oils, mixed with the matrix, meso-tetrakis(pentafluorophenyl)porphyrin, provided reproducible MALDI-TOF spectra in which the ions were dominated by sodiated sodium carboxylates [RCOONa + Na]+. Thus, palm kernel oil was found to contain capric acid, lauric acid, myristic acid, palmitic acid, oleic acid, and stearic acid. Palm oil had a fatty acid profile including palmitic, linoleic, oleic, and stearic. The relative percentages of the fatty acids in olive oil were palmitoleic (1.2 +/- 0.5), palmitic (10.9 +/- 0.8), linoleic (0.6 +/- 0.1), linoleic (16.5 +/- 0.8), and oleic (70.5 +/- 1.2). For soybean oil, the relative percentages were: palmitoleic (0.4 +/- 0.4), palmitic (6.0 +/- 1.3), linolenic (14.5 +/- 1.8), linoleic (50.1 +/- 4.0), oleic (26.1 +/- 1.2), and stearic (2.2 +/- 0.7). This method was also applied to the analysis of two commercial soap formulations. The first soap gave a fatty acid profile that included: lauric (19.4% +/- 0.8), myristic (9.6% +/- 0.5), palmitoleic (1.9% +/- 0.3), palmitic (16.3% +/- 0.9), linoleic (5.6% +/- 0.4), oleic (37.1% +/- 0.8), and stearic (10.1% +/- 0.7) and that of the second soap was: lauric (9.3% +/- 0.3), myristic (3.8% +/- 0.5), palmitoleic (3.1% +/- 0.8), palmitic (19.4% +/- 0.8), linoleic (4.9% +/- 0.7), oleic (49.5% +/- 1.1), and stearic (10.0% +/- 0.9). The MALDI-TOFMS method described in this communication is simpler and less time-consuming than the established transesterification method that is coupled with analysis by gas chromatography/mass spectrometry (GC/MS). The new method could be used routinely to determine the qualitative fatty acid composition of vegetable oils, and, when fully validated by comparison with standard analytical methodologies, should provide a relatively fast quantitative measurement of fatty acid mixtures and/or soap formulations that contain saturated and unsaturated hydrocarbon moieties.

Esterification↗