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PubMed1989

Specific high affinity binding of lipoxygenase metabolites of arachidonic acid by liver fatty acid binding protein.

Liver fatty acid binding protein (L-FABP) binds avidly the arachidonic acid metabolites, hydroperoxyeicosatetraenoic acids (HPETEs) and hydroxyeicosatetraenoic acids (HETEs). Binding of 15-[3H]HPETE was specific, saturable, reversible, and rapid. Protein specificity was indicated by the following order: L-FABP greater than bovine serum albumin greater than ovalbumin = beta-lactoglobulin greater than ribonuclease. Ligand specificity was evidenced by the following order of apparent competition: 15-HPETE greater than or equal to 5-HETE greater than or equal to 5-HPETE = oleic acid greater than 12-HETE greater than 12-HPETE greater than or equal to 15-HETE greater than prostaglandin E1 much greater than leukotriene C4 greater than prostaglandin E2 much greater than thromboxane B2 = leukotriene B4. Once bound, 15-HPETE was reversibly displaced. Ligand was recovered from the protein complex and confirmed to be 15-[3H]HPETE by TLC. L-FABP bound HPETE with a dissociation constant of 76 nM,5-HETE at 175 nM, and 15-HETE at 1.8 microM, and the reference fatty acids oleic acid at 1.2 microM and arachidonic acid at 1.7 microM. Thus, the affinity was approximately 16-fold greater for 15-HPETE, and 7-fold higher for 5-HETE, than for oleic acid. The need exists for studies of complexes of L-FABP with the HPETEs and HETEs in hepatocytes, especially since L-FABP has previously been associated with mitosis in normal hepatocytes, and shown to be the target protein of two liver carcinogens, and these arachidonic acid metabolites have been found to be able to modulate activities related to cell growth.

Animals↗
PubMedDate not supplied

Vascular effects of non-esterified fatty acids: implications for the cardiovascular risk factor cluster.

Insulin resistance emerges as a central component of the risk factor cluster and is a likely contributor to vascular disease independently of traditional risk factors such as hypertension and diabetes mellitus. However, the intermediary mechanisms by which atherosclerosis is accelerated among patients with the insulin resistance syndrome remain inadequately defined. Most of the attention has centered on hyperinsulinemia and defects of insulin-mediated glucose disposal. However, we observed that obese hypertensive patients have elevated plasma concentrations of non-esterified fatty acids (NEFAs), including oleic acid, which are highly resistant to suppression by insulin. Resistance to insulin's fatty acid lowering action correlate with blood pressure in obese subjects independently of defects in glucose disposal. This observation raises the possibility that NEFAs have biologically significant effects on the cardiovascular system. In fact, oleic acid impairs nitric oxide synthase activity and endothelium-dependent vasorelaxation in vitro. Moreover, raising NEFAs in normal human volunteers to levels observed in obese hypertensive patients impairs lower extremity endothelium-dependent vasodilation and augments local and systemic vascular alpha1-adrenoceptor reactivity in normal volunteers. Thus, raising NEFAs replicates in healthy subjects important functional vascular changes implicated in the hypertension and atherosclerosis observed in patients with the risk factor cluster. At a molecular level, experiments in cultured vascular smooth muscle cells demonstrate that oleic acid activates a mitogenic signaling cascade which includes protein kinase C, reactive oxygen species and extracellular signal-regulated kinases. Each of these signaling events has been implicated in the structural and functional vascular changes which accompany the risk factor cluster. Collectively, these observations raise the possibility that fatty acids contribute to functional and structural vascular changes among insulin-resistant individuals. A better understanding of the signaling mechanisms by which NEFAs exert their vascular effects may facilitate novel and more effective therapeutic approaches to managing the cardiovascular risk factor cluster.

Animals↗
PubMed2002

Lithium dilution cardiac output measurement in oleic acid-induced pulmonary edema.

OBJECTIVE: To determine whether lung injury influences the accuracy of lithium dilution cardiac output (CO) measurement. DESIGN: Animal experimental study. SETTING: Animal experimental laboratory. PARTICIPANTS: Swine (n = 23) weighing 26.4 +/- 2.47 kg (mean +/- SD). INTERVENTIONS: The animals were anesthetized and tracheotomized, then a pulmonary artery catheter was inserted into the right jugular vein, and a catheter (18G) was placed in the femoral artery. After median sternotomy and pericardiotomy, a left ventricular catheter (18G) was directly inserted. CO was measured by giving a bolus injection of lithium chloride into either the right atrium or the left ventricle in each animal. After control measurements, permeability pulmonary edema was initiated by infusing oleic acid into the central vein (injury). About 2 hours after oleic acid infusion, CO measurements were repeated in the same manner as the control measurement had been taken. MEASUREMENTS AND MAIN RESULTS: Under each condition, right atrium lithium injection was similar to left ventricle lithium injection. The mean of these differences at injury (-0.06 +/- 0.55 L/min) was the same as that at control (-0.05 +/- 0.36 L/min). CONCLUSIONS: Although the variability of lithium dilution CO measurement after oleic acid-induced pulmonary edema was greater than that of the control, this technique was acceptable even in cases of lung injury.

Animals↗
PubMed1985

Vasoactive intestinal polypeptide, cholecystokinin, glucagon, and bile-oleate-induced jejunal hyperemia.

The purpose of this study was to evaluate the roles of vasoactive intestinal polypeptide (VIP), cholecystokinin (CCK), and glucagon in the local regulation of the lipid-induced intestinal hyperemia. Total blood flow and the arteriovenous hormone concentration gradient were measured in isolated jejunal loops of anesthetized dogs with either saline, bile (10% in normal saline), oleic acid (40 mM in normal saline), or oleic acid and bile in the lumen. The bile-oleic acid mixture increased both blood flow (+21 +/- 7%) and VIP release (+118 +/- 7%), while CCK release was considerably less. There was a transient rise in glucagonlike immunoreactivity but no change in pancreatic glucagon release. Neither bile nor oleic acid alone altered either local blood flow or hormone release. Infusion of VIP into the arterial circulation of the jejunum significantly reduced vascular resistance (-11 +/- 4%) but at a dose (150 ng . min-1 X 100 g-1) 10 times that released in response to the bile-oleic acid mixture. This study indicates that oleic acid increases both blood flow and intestinal hormone production only when present in the lumen in micellar form and suggests that VIP could play a role in the jejunal vascular response to fat.

Animals↗
PubMed1975

The effect of essential fatty acid deficiency upon fatty acid uptake by the brain.

Young adult rats, either control or essential fatty acid deficient, were administered either [3-H] oleic acid or [3-H] arachidonic acid by stomach tube. In addition, a group of control rats was given [3-H] palmitic acid. The rats were killed at various times therafter, and the radioactivity of the lipids of brain and plasma was examined. In confirmation of previous work, the blood lipid label was found to rise rapidly and then fall, wheras the activity of brain lipids increased slowly and did not show a decline through the 24-h period studied. Analysis of the brain uptake data according to first-order kinetics confirmed the impressions gained from visual inspection of the data. The initial rate of uptake of arachidonic acid was about 4.5 times that of oleic acid in control animals and in deficient animals. Essential fatty acid deficiency, however, did not induce an altered rate of uptake for either oleic acid or arachidonic acid. The rate of uptake of palmitic acid by control rats was not significantly different from that of oleic acid. Even though the initial rates of incorporation of oleic and arachidonic acids were not changed during essential fatty acid deficiency, the final levels of radioactivity obtained in brain lipids were higher in deficient rats with both fatty acids. The plateau value obtained with oleic acid was 1.5 times higher in deficient animals, while the plateau value for arachidonic acid was 1.7 times higher. An experiment in which deficient animals were allowed access to a control diet for 12 or 24 h prior to the labeling experiment suggested that the higher levels of radioactivity found in brain lipids of deficient animals was not due to an isotope dilution effect. Such animals still displayed the labeling pattern of deficient animals with arachidonic acid, while the results with oleic acid varied somewhat. Our results suggest that essential fatty acid deficiency does not alter the ability of the brain to take up the fatty acids studied. However, the fatty acids, especially arachidonic, are retained in the brain to a greater extent in the deficient animals.

Animals↗
PubMed1984

CTP:phosphorylcholine cytidylyltransferase in rat lung. The effect of free fatty acids on the translocation of activity between microsomes and cytosol.

Phosphatidylglycerol and oleic acid had differential effects on cytidylyltransferase activity in cytosol and microsomes. The low-molecular-weight cytidylyltransferase in cytosol was stimulated more by phosphatidylglycerol than by oleic acid, whereas microsomal activity was stimulated more by oleic acid than by phosphatidylglycerol. Microsomal activity was stimulated by several unsaturated fatty acids but was not stimulated by saturated fatty acids. Bovine serum albumin decreased cytidylyltransferase activity in microsomes in the presence or absence of oleic acid but did not alter the activity measured in the presence of phosphatidylglycerol. The addition of oleic acid to albumin/microsome mixtures in amounts exceeding the binding capacity of albumin lead to complete recovery of the oleic acid stimulation. The addition of oleic acid to postmitochondrial supernatants resulted in a translocation of cytidylyltransferase activity from cytosol to microsome. The magnitude of the shift was severalfold greater with fetal preparations than adult. The free fatty acid content of microsomes increased coincident with the translocation. Bovine serum albumin, added to postmitochondrial supernatants, caused a release of cytidylyltransferase from microsomes to cytosol and a corresponding decrease in microsomal free fatty acid content. The amount of cytidylyltransferase activity in microsomes increased shortly after birth. The increase was accompanied by an increase in free fatty acid content of the microsomes. The increase in cytidylyltransferase activity and free fatty acids which occurred in vivo following birth was nearly identical to that obtained by adding oleic acid to postmitochondrial supernatants from fetal lung. We conclude that free fatty acids may affect the intracellular activity of cytidylyltransferase by promoting the translocation of inactive cytosolic forms to microsomes as well as by stimulating microsomal bound activity.

Aging↗
PubMed1993

Inhibition of lymphocyte protein kinase C by unsaturated fatty acids.

Oleic, arachidonic, eicosapentaenoic and docosahexaenoic acids inhibited lymphocyte protein kinase C activity in the presence of Ca2+, phospholipid and a phorbol ester. Linoleic and alpha-linolenic acids did not affect protein kinase C activity in this way and none of the fatty acids affected protein kinase A activity. These findings indicate direct inhibitory effects of some unsaturated fatty acids upon protein kinase C. Culture of lymphocytes in the presence of oleic, arachidonic, eicosapentaenoic or docosahexaenoic acids resulted in a reduction in protein kinase C activity (by up to 45%). Culture with linoleic or alpha-linolenic acids did not affect protein kinase C activity and none of the fatty acids affected total protein kinase A activity or the percentage in the active form. These results show for the first time that fatty acids have long term effects upon protein kinase C activity, perhaps as a result of altering the rate of turnover of the enzyme. It is suggested that the inhibition of lymphocyte functions caused by unsaturated fatty acids may in part be due to their effect on protein kinase C.

Animals↗
PubMed2000

Sodium nitroprusside mitigates oleic acid-induced acute lung injury.

BACKGROUND: Acute lung injury (ALI) is associated with pulmonary hypertension, intrapulmonary shunting, and increased microvascular permeability, leading to altered oxygenation capacity. Oleic acid (OA) creates a significant ALI that physiologically mimics human adult respiratory distress syndrome (ARDS). It has been hypothesized that pulmonary vasodilatation may improve ALI. Studies in our laboratory using this model and nitric oxide (NO) have shown that NO inhalation is detrimental and worsens the effects of OA. We studied the effect of pretreatment with a potent vasodilator, sodium nitroprusside (SNP), on ALI induced by OA in an isolated lung model. We hypothesized that pretreatment with SNP will worsen pulmonary hypertension and oxygenation in OA-induced ALI, similar to the effects seen with inhaled NO in this model. METHODS: Rabbit heart lung blocks were isolated, flushed in vivo, harvested, immediately perfused with whole blood, and ventilated with 50% oxygen. Pulmonary artery pressure was determined every 15 seconds for 90 minutes of perfusion. Oxygenation was determined by blood gas analysis of pulmonary venous effluent at 0, 20, 40, 60, and 90 minutes after initiation of OA infusion. Four groups were studied: saline control (SC), oleic acid control (OAC; 20-minute infusion of 50% OA/ethanol into pulmonary circulation), SNP control (NPC; 10 microg/ kg/min SNP infused without subsequent OA infusion), and SNP treatment (NPRx); 10 microg/kg/min SNP infused before OA/ethanol. Pulmonary artery pressure (PAP), oxygenation (arterio-venous oxygen difference [AVO2], compliance (CPL), and wet/dry lung weight were determined. RESULTS: No significant differences were found between the NPRx group and SC. Pretreatment with SNP eliminated the detrimental effects of OA infusion. CONCLUSIONS: Contrary to our hypothesis, pretreatment with SNP eliminates the decrease in oxygenation and increase in lung weight, and ameliorates pulmonary hypertension in our isolated lung model of OA-induced ALI.

Animals↗
PubMed2000

Effects of dietary alpha-linolenic acid on the conversion and oxidation of 13C-alpha-linolenic acid.

The effects of a diet rich in alpha-linolenic acid vs. one rich in oleic acid on the oxidation of uniformly labeled 13C-alpha-linolenic acid and its conversion into longer-chain polyunsaturates (LCP) were investigated in vivo in healthy human subjects. Volunteers received a diet rich in oleic acid (n = 5) or a diet rich in alpha-linolenic acid (n = 7; 8.3 g/d) for 6 wk before and during the study. After 6 wk, subjects were given 45 mg of 13C-alpha-linolenic acid dissolved in olive oil. Blood samples were collected at t = 0, 5, 11, 24, 96, and 336 h. Breath was sampled and CO2 production was measured each hour for the first 12 h. The mean (+/- SEM) maximal absolute amount of 13C-eicosapentaenoic acid (EPA) in plasma total lipids was 0.04 +/- 0.01 mg in the alpha-linolenic acid group, which was significantly lower (P = 0.01) than the amount of 0.12 +/- 0.03 mg 13C-EPA in the oleic acid group. Amounts of 13C-docosapentaenoic acid (DPA) and 13C-docosahexaenoic acid (DHA) tended to be lower as well. The mean proportion of labeled alpha-linolenic acid (ALA) recovered as 13CO2 in breath after 12 h was 20.4% in the ALA and 15.7% in the oleic acid group, which was not significantly different (P = 0.12). The cumulative recovery of 13C from 13C-ALA in breath during the first 12 h was negatively correlated with the maximal amounts of plasma 13C-EPA (r = -0.58, P = 0.047) and 13C-DPA (r = -0.63, P = 0.027), but not of 13C-DHA (r = -0.49, P = 0.108). In conclusion, conversion of 13C-ALA into its LCP may be decreased on diets rich in ALA, while oxidation of 13C-ALA is negatively correlated with its conversion into LCP. In a few pilot samples, low 13C enrichments of n-3 LCP were observed in a diet rich in EPA/DHA as compared to oleic acid.

Adult↗
PubMed1985

The transfer of free fatty acids across the human placenta.

Thirty-three matched maternal venous and umbilical cord vein and artery plasma samples were obtained at elective caesarean section and the concentrations of the individual free fatty acids determined. The maternal levels were 1.009 (SEM 0.043) and the umbilical vein-artery difference was 0.036 (SEM 0.011) mmol/l. There was a significant correlation between the mean concentration in maternal venous blood and the vein-artery difference for myristic, palmitic, stearic, linoleic and docosahexaenoic acids but not for oleic acid. When arachidonic acid concentration in the fetus was high, then the vein-artery difference was negative (flow to the placenta), when it was low, the difference was positive (flow to the fetus). Thus whilst there appears in general to be a flow of fatty acid to the fetus dependent on maternal free fatty acid concentrations, the transfer of arachidonic acid is largely determined by other factors. The reasons why oleic acid does not behave like the other fatty acids is not clear.

Adolescent↗
PubMed1986

Concentrations of secretin and CCK in plasma and pancreatico-biliary secretion in response to intraduodenal acid and fat.

To study the effect of emulsified oleic acid on pancreatic secretion and concentrations of secretin and cholecystokinin (CCK) in plasma, eight normal subjects received three sets of duodenal perfusates containing peptone pH 6.0 or pH 2.7, with and without 20 mM oleic acid. Pancreatic secretion was measured by an indicator dilution technique. At pH 6.0, peptone and oleic acid was about as effective as peptone pH 2.7 in stimulating secretin release. However, oleic acid in addition produced a three-fold increase in plasma CCK and was five times as effective as pH 2.7 in stimulating duodenal flow. Also, at pH 2.7, oleic acid augmented pancreatic secretion and concentrations of CCK and secretin in plasma. Duodenal output of amylase and bile salts was independent of the pH of infusate. Low pH alone was a very weak stimulant of CCK release and did not stimulate output of amylase and bile. Emulsified oleic acid is a potent releaser of secretin and CCK and augments the acid-induced pancreatic secretion.

Adult↗
PubMed2006

Short-term and long-term effects of fatty acids in rat hepatoma AS-30D cells: the way to apoptosis.

Arachidonic acid and, to a smaller extent, oleic acid at micromolar concentrations decreased the mitochondrial membrane potential within AS-30D rat hepatoma cells cultivated in vitro and increased cell respiration. The uncoupling effect of both fatty acids on cell respiration was partly prevented by cyclosporin A, blocker of the mitochondrial permeability transition pore. Arachidonic acid increased the rate of reactive oxygen species (ROS) production, while oleic acid decreased it. Both fatty acids induced apoptotic cell death of AS-30D cells, accompanied by the release of cytochrome c from mitochondria to the cytosol, activation of caspase-3 and association of proapoptotic Bax protein with mitochondria; arachidonic acid being a more potent inducer than oleic acid. Trolox, a potent antioxidant, prevented ROS increase induced by arachidonic acid and protected the cells against apoptosis produced by this fatty acid. It is concluded that arachidonic and oleic acids induce apoptosis of AS-30D hepatoma cells by the mitochondrial pathway but differ in the mechanism of their action: Arachidonic acid induces apoptosis mainly by stimulating ROS production, whereas oleic acid may contribute to programmed cell death by activation of the mitochondrial permeability transition pore.

Animals↗
PubMed1992

Comparison of effects of lauric acid and palmitic acid on plasma lipids and lipoproteins.

The effects of lauric acid (C12:0) on plasma lipids and lipoproteins were compared with the effects of palmitic acid (C16:0) and oleic acid (C18:1) in a metabolic-diet study of 14 men by using liquid-formula diets fed for 3 wk each in random order. Lauric acid was supplied in a synthetic high-lauric oil, palmitic acid was provided by palm oil and oleic acid in oleic-rich sunflower seed oil. The high-lauric oil resulted in higher concentrations of plasma total cholesterol (4.94 +/- 0.75 mmol/L [mean +/- SE]) and LDL cholesterol (3.70 +/- 0.57 mmol/L) when compared with high-oleic sunflower oil (4.44 +/- 0.54 and 3.31 +/- 0.44 mmol/L, respectively), but did not raise total and LDL cholesterol concentrations as much as did palm oil (5.17 +/- 0.65 and 3.93 +/- 0.51 mmol/L, respectively). No differences were noted in plasma triglycerides or HDL cholesterol. Lauric acid raises total and LDL cholesterol concentrations compared with oleic acid, but is not as potent for increasing cholesterol concentrations as is palmitic acid.

Adult↗
PubMed1993

Presence of carnitine acetyltransferase in peroxisomes and in mitochondria of oleic acid-grown Saccharomyces cerevisiae.

Activity of carnitine acetyltransferase was detected in glucose- and oleic acid-grown Saccharomyces cerevisiae. Oleic acid-grown cells showed a ten-fold higher activity than glucose-grown cells. Subcellular fractionation of oleic acid-grown cells showed that carnitine acetyltransferase was present in peroxisomes, mitochondria, and cytosol. The results suggested the plausible presence of an 'acetylcarnitine shuttle' in this yeast, as in the case of an n-alkane-assimilating yeast, Candida tropicalis.

Acetyl Coenzyme A↗
PubMed1989

Fatty acids and cholesterol: effect on the interaction of theophylline with bovine serum albumin.

The binding of theophylline (Th, 11-840 microM) to bovine serum albumin (BSA, 10 microM) using microdialysis technique in the presence of fatty acids (2.5-50.0 microM) and cholesterol (20-500 nM) indicates that fatty acids and cholesterol inhibit the binding of Th to BSA. The maximum inhibition (90.5%) occurs in presence of acetic acid (AA) followed by lauric acid (LA, 83.3%), palmitic acid (PA, 72.2%), oleic acid (OA, 44.4%) and cholesterol (22.2%). Fatty acids and cholesterol also decrease the number of binding sites and the affinity for the binding of Th to BSA. Such a decrease is maximum in the presence of AA followed by LA, PA, OA and cholesterol. Complete abolition of the low affinity binding site in the presence of AA indicates that the low affinity binding is predominantly ionic in nature while the high affinity binding involves ionic and other type(s) of unidentified force(s). This makes high affinity binding stronger than low affinity binding.

Acetates↗
PubMed1992

Research note: eggshell quality in Japanese quail fed different fatty acids.

The purpose of the present study was to determine the effects of diets containing 3% palmitic acid (Diet PA), oleic acid (Diet OA), or linoleic acid (Diet LA) on the shell quality of eggs of Japanese quail. Each diet was fed to 10 hens maintained individually in wire quail laying cages. There was no difference (P greater than .05) in feed consumption between hens fed Diets OA and LA, but hens of both groups consumed less (P less than .05) feed than those fed Diet PA. Egg weight, shell weight, and thickness of shell plus membrane were not influenced by dietary treatment (P greater than .05). However, specific gravity of eggs from hens fed Diet OA was significantly higher (P less than .05) than that of eggs from those fed either Diet PA or Diet LA. Comparison of these data with hatchability data obtained in a previous experiment conducted under similar conditions suggests that the differences in hatchability would not be explained by differences in eggshell quality.

Animals↗
PubMed2001

Behenic acid is a cholesterol-raising saturated fatty acid in humans.

BACKGROUND: Dietary behenic acid (22:0) is poorly absorbed. Because of its low bioavailability compared with other fatty acids and because of its very long chain length, the effect of dietary behenic acid (behenate) on serum lipid concentrations in humans is assumed to be neutral. OBJECTIVE: The objective was to establish the cholesterol-raising potential of behenic acid by comparing the effects on lipid and lipoprotein concentrations of a specially formulated fat enriched with behenic acid with those of palm oil (rich in palmitic acid; 16:0) and high-oleic acid sunflower oil (rich in cis oleic acid; 18:1). DESIGN: In a randomized, crossover, metabolic-ward study, 7 mildly hypercholesterolemic men were fed 3 natural-food diets supplemented with behenate oil, palm oil, or high-oleic acid sunflower oil. Mean serum lipid and lipoprotein concentrations and plasma triacylglycerol fatty acid composition were determined from fasting blood drawn during the final 4 d of each 3-wk diet period. RESULTS: Behenate oil produced mean concentrations of total cholesterol (5.87+/-0.8 mmol/L) and LDL cholesterol (4.40+/-0.8 mmol/L) not significantly different from those produced by palm oil (5.84+/-0.7 and 4.42+/-0.7 mmol/L, respectively) but significantly higher than those produced by high-oleic acid sunflower oil (5.12+/-0.5 and 3.70+/-0.6 mmol/L, respectively). There were no significant differences in triacylglycerol or HDL-cholesterol concentrations. CONCLUSIONS: Despite its low bioavailability compared with oleic acid, behenic acid is a cholesterol-raising fatty acid in humans and is therefore not a suitable substitute for palmitic acid in manufactured triacylglycerols.

Aged↗
PubMed1985

Differential effect of cyclooxygenase inhibitors on absorptive hyperemia.

To test whether the hydrolytic products of digestion could stimulate vasoactive prostaglandin synthesis in the intestine, the muscularis and mucosa of the rat jejunum were suffused with a bicarbonate-buffered Ringer vehicle containing cyclooxygenase inhibitors (meclofenamate or indomethacin; 3 X 10(-5) M). To evoke blood flow changes, either glucose (56 mM), oleic acid (20 or 40 mM), or sodium arachidonate was added to the mucosal vehicle. Bile salt (taurocholic acid, 10 mM) was added to emulsify oleic acid. Blood flow was calculated (BFc) in submucosal arterioles by use of video microscopy. Neither bile salt nor cyclooxygenase inhibitors altered resting BFc. Neither oleic acid concentration nor solution osmolality altered the magnitude of absorptive hyperemia. After 10 min of glucose, BFc increased 36 +/- 6% with vehicle (n = 16) and 39 +/- 8% with meclofenamate (n = 10). After 10 min of oleic acid, BFc increased 21 +/- 5% with vehicle (n = 17) and 34 +/- 6% with inhibitors (n = 17). In animals exposed twice to the same concentration of oleic acid, the paired difference between the vehicle and inhibitors (19 +/- 7%; n = 9) was significant. Arachidonate alone produced no dose-related (0.06-1.9 mM) effect on BFc (n = 41), but arachidonate (0.3 mM) combined with cyclooxygenase inhibitors (6 X 10(-5) M) produced a significant BFc increase of 35 +/- 7% (n = 6). These observations suggest that the absorption of oleic acid, but not glucose, stimulates the synthesis of a vasoactive metabolite of arachidonate. The mechanism for the differential effect of cyclooxygenase inhibitors is unknown but could involve nonprostaglandin metabolites of arachidonate, such as lipoxygenase or cytochrome P-450 products.

Animals↗