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PubMed1973

Dietary intake of linoleic acid in multiple sclerosis and other diseases.

The linoleic acid intake of patients with multiple sclerosis is not significantly different from that of healthy control subjects. This is true both in absolute terms and when linoleic acid intake is expressed as a percentage of total fat intake. In the other categories of illness, included as control groups, linoleic acid intake was significantly decreased only in patients with acute non-neurological illness and in this case only when considered in absolute terms. In all groups studied the daily linoleic acid intake was in excess of 1·7% of the total calorie intake and in the case of multiple sclerosis was 2·7% of the total calories ingested. Since other workers have shown that linoleic acid absorption is not altered in multiple sclerosis and we have shown that the diet is not deficient, it seems that the decrease in linoleic acid content is due to some process occurring after the absorption of this essential fatty acid.

Adult↗
PubMed1993

bis-Allylic hydroxylation of linoleic acid and arachidonic acid by human hepatic monooxygenases.

[14C]Linoleic acid was incubated with human liver microsomes and NADPH and biosynthesis of allylic hydroxy fatty acids was investigated. 11-Hydroxy-9Z,12Z-octadecadienoic acid (11-HODE), 9-hydroxy-10E,12Z-octadecadienoic acid (9-HODE), 13-hydroxy-9Z,11E-octadecadienoic acid (13-HODE) and 14-hydroxy-9Z,12Z-octadecadienoic acid were identified. 9-HODE and 13-HODE were formed with stereoselectivity (80% R) provided that 11-HODE was prevented from decomposing to 9(R,S)-HODE and 13(R,S)-HODE by extractive isolation at pH 5-6. Human hepatic microsomes metabolized [14C]arachidonic acid to many products, including 13-HETE and small amounts of 15-HETE (> 90% R), 11-HETE (59% R) and 12-HETE (> 90% R). Hepatic microsomes of untreated rats metabolized [14C]linoleic acid to 11-HODE as a major product, but significant formation of 11-HODE by purified cytochrome P-450 (P450) (CYP1A1, CYP2B1, CYP2B4, CYP2E1, CYP3A6 and CYP4A1) in a reconstituted system could not be detected, indicating that 11-HODE might be formed by other and constitutive P450 isozymes.

Animals↗
PubMed1991

Studies on bio-antioxidants--prooxidation of vitamin E on the autoxidation of linoleic acid in sodium dodecyl sulfate micelles.

The reaction of vitamin E (alpha-tocopherol) with linoleic acid containing peroxidized linoleic acid has been studied. No significant reaction was found in ethanol solution, whereas in sodium dodecyl sulfate micelles vitamin E reacted rapidly with peroxidized linoleic acid, and thereby induced the peroxidation of linoleic acid, leading to oxygen absorption. The reaction kinetics was studied in detail by u.v. spectroscopy, HPLC and ESR spectroscopy. It was found that the main product was alpha-tocopherone with alpha-tocopheroxy radical as the reaction intermediate. A mechanism involving two consecutive bimolecular reactions between peroxidized linoleic acid and alpha-tocopherol and between peroxidized linoleic acid and alpha-tocopheroxy radical, with rate constant 2.93 and 6.21 mol/L-1s-1 respectively is proposed. The micellar effect on the reaction is discussed.

Antioxidants↗
PubMed1998

Hydration of linoleic acid by bacteria isolated from ruminants.

Two strains of Enterococcus faecalis isolated from the ovine rumen and known to hydrate oleic acid were shown to transform linoleic acid by hydration into two products. The products, identified as 10-hydroxy-12-octadecenoic acid and 13-hydroxy-9-octadecenoic acid, were formed during stationary phase in yields of 13% and 6% respectively. Yields increased to 22% and 14% when culture conditions were optimised. To our knowledge, this is the first report of 13-hydroxy-9-octadecenoic acid production by bacteria. During a search for further linoleic-acid-hydrating bacteria, a strain of Streptococcus bovis isolated from bovine faeces and the ruminal strain S. bovis JB1 were found to hydrate linoleic acid. Both strains formed only one product and the most rapid appearance occurred during exponential growth. The S. bovis product, identified as 13-hydroxy-9-octadecenoic acid, formed in a yield of 28%. This study provides the first information on linoleic acid hydration by ruminal bacteria.

Animals↗
PubMed1995

Comparison of hypocholesterolemic effects induced by dietary linoleic acid and oleic acid in hamsters.

We investigated the differences between the hypocholesterolemic effects induced by dietary linoleic acid and those induced by oleic acid in hamsters. Addition of 5% linoleic acid or oleic acid to a 0.1% cholesterol-supplemented diet diminished the increases in plasma total and low density lipoprotein (LDL) cholesterol induced by cholesterol alone. Linoleic acid decreased high density lipoprotein (HDL) cholesterol in comparison with cholesterol alone, whereas oleic acid did not. As compared with a standard diet or a cholesterol-supplemented diet, linoleic acid and oleic acid each prevented hepatic LDL receptor suppression, although linoleic acid was more effective. Oleic acid prevented the increase in plasma cholesteryl ester transfer protein (CETP) activity induced by dietary cholesterol, whereas linoleic acid did not. Neither linoleic acid nor oleic acid altered hepatic 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase activity. Only oleic acid increased hepatic cholesterol 7 alpha-hydroxylase activity. These results suggest that dietary linoleic and oleic acids diminish the cholesterol-induced increases in plasma total and LDL-cholesterol by preventing hepatic LDL receptor suppression, and in the case of oleic acid by also preventing the increase in the plasma CETP activity. These effects on cholesterol 7 alpha-hydroxylase activity may influence bile lipid metabolism.

Animals↗
PubMed1995

Survey of the conjugated linoleic acid contents of dairy products.

The objective of this research was to determine the content of conjugated linoleic acid, an anticarcinogen, in dairy products. Fifteen cheeses, three fermented dairy products (other than cheeses), and four fluid milk products (two brands for each product) were included in the survey. Total lipids, fatty acids, protein, moisture, and titratable acidity were also measured to determine the relationship between the content of these constituents and conjugated linoleic acid content. The conjugated linoleic acid content of cheeses ranged from 3.59 to 7.96 mg/g of lipid. Blue, Brie, Edam, and Swiss cheeses had significantly higher conjugated linoleic acid content than the other cheeses. Sharp Cheddar cheeses tended to have higher conjugated linoleic acid content than the medium Cheddar cheeses, but the increase was not significant. The conjugated linoleic acid content of the other fermented dairy products ranged from 3.82 to 4.66 mg/g of lipid, and cultured buttermilk had the highest content. The conjugated linoleic acid contents of four fluid milks ranged from 3.38 to 6.39 mg/g of lipid and were not significantly different from one another. Multiple linear regressions of conjugated linoleic acid content and the total fatty acid content indicated a relationship between conjugated linoleic acid content and the content of precursors and intermediates of conjugated linoleic acid formation, including linoleic and oleic acids.

Animals↗
PubMed2000

Metabolism of n -9, n -6 and n -3 fatty acids in hepatoma Morris 7777 cells. Preferential accumulation of linoleic acid in cardiolipin.

The objective of this study was to investigate, using a pulse-chase technique, the different incorporation of (1-(14)C) n -9, n -6 and n 3 fatty acids into hepatoma lipids and their secretion to the culture medium. Docosahexaenoic acid (DHA) accumulated preferentially into the triacylglycerol while arachidonic acid (AA) did into the phospholipid fraction. DHA was poorly secreted to the culture medium whereas AA was secreted to a large extent. The fatty acids were initially esterified mainly into phosphatidylcholine and phosphatidylethanolamine. During the 24 h chase, a general shift from phosphatidylcholine to phosphatidylethanolamine was observed. Linoleic acid was esterified in cardiolipin to a much greater extent than any other fatty acid and it was not converted to more polyunsaturated fatty acids. The supplementation of the culture medium with polyunsaturated fatty acids had no inhibitory effect on the growth of the hepatoma cells, in marked contrast to observations made in other tumoral cells. The reasons for the resistance of the hepatoma cells to polyunsaturated fatty acid toxicity, including the possible antioxidant effect of linoleic acid accumulation in cardiolipin, are also discussed.

Albumins↗
PubMed1999

Recent advances in conjugated linoleic acid research.

New results on the physiological properties of conjugated linoleic acid have been published by several working groups, especially showing the effects of single conjugated linoleic acid isomers on carcinogenesis and body composition. Recently, other studies have shown that conjugated linoleic acid has an influence on diabetes mellitus, platelet aggregation and the immune system. Conjugated linoleic acid was found to modify prostaglandin metabolism and delta9-desaturase activity and influence apoptosis. Furthermore, improved analytical methods using 13C nuclear magnetic resonance and silver ion high performance liquid chromatography are available to investigate the composition of conjugated linoleic acid mixtures and the exact structure of separated isomers. Also, the synthesis of isolated isomers is described, as published by different authors, in order to determine further the effects of each single conjugated linoleic acid isomer. In addition, new data on the contents of conjugated linoleic acid in foods, human adipose tissue and fluids are given in this review. More data need to be obtained using isolated isomers, with particular emphasis on studies in humans.

Adipose Tissue↗
PubMed1980

Cardiovascular effects of dietary linoleic acid.

A survey is given of the effects of a linoleic-acid-rich diet on arterial thrombosis, blood platelet function and blood pressure in rats and man, and on coronary flow rate and heart muscle function of isolated rat hearts. Dietary linoleic acid decreases arterial thrombosis tendency in a dose-dependent manner in rats, as measured by the aorta loop technique. In a group of patients, a linoleic-acid-rich diet improved blood platelet aggregation measured with the filtragometer as compared with a similar group which was given a linoleic-acid-poor diet. The patients who received a high linoleic acid diet showed a lower cardiovascular death rate than the low linoleic acid group. Salt-induced hypertension in rats can be prevented and cured by a high linoleic acid diet. In man, the results of a few experiments show a decreasing tendency of blood pressure during a diet enriched with linoleic acid. In the isolated hearts of rats fed a diet high in linoleic acid, coronary flow and heart muscle function both increase as compared to control groups fed lard or hardened coconut oil. The observed effects are discussed against the background of recent findings in the field of prostaglandin research.

Animals↗
PubMed1984

[Contribution of linoleic acid to the bitter taste of poppy seeds (Papaver somniferum)].

In lipids isolated from poppy seeds which tasted "burning-bitter" the off-taste was associated with the free fatty acids fraction. In this fraction linoleic acid predominates, while oxidized fatty acids were among the minor constituents. The taste threshold of linoleic acid emulsified in water with monolinolein lies in the range of 4.0-6.0 mumol/ml. On the basis of its high concentration and relatively low taste threshold we conclude that free linoleic acid contributes significantly to the "burning-bitter" off-taste in poppy seeds.

Chromatography, Gel↗
PubMed1995

Steady-state rates of linoleic acid biohydrogenation by ruminal bacteria in continuous culture.

Ruminal biohydrogenation of linoleic acid was determined in fermenters with a continuous culture of microorganisms. Rates of biohydrogenation and changes of fatty acids in culture were measured during steady-state concentration of linoleic acid that was achieved by continuous infusion of linoleic acid into the fermenters. A number of trans and cis isomers were identified using a GLC equipped with an infrared detector. The infusion of linoleic acid resulted in a substantial increase in the content of trans-C18:1 and a lesser increase in cis-C18:1. the major trans peak consisted of a mixture of n-9 and n-7 isomers. Biohydrogenation of infused linoleic acid averaged 77%. There was evidence of fatty acid loss, as determined by a decrease in the recovery of linoleic acid after 8 h of infusion. Addition of C18:2n-6 had no major effect on the VFA production by ruminal microorganisms. The results were similar to those measured in vivo, indicating that artificial fermenters were reliable predictors of fatty acid metabolism in vivo.

Animal Feed↗
PubMed1974

The enzymic and non-enzymic degradation of colneleic acid, an unsaturated fatty acid ether intermediate in the lipoxygenase pathway of linoleic acid oxidation in potato (Solanum tuberosum) tubers.

Colneleic acid is an unsaturated ether fatty acid derived from linoleic acid via a lipoxygenase-mediated enzyme pathway. It is degraded (a) by an enzyme in potato tubers which is heat-labile and non-dialysable and (b) by a model system containing catalytic amounts of Fe(2+) ions. Both enzyme- and Fe(2+)-catalysed systems have similar properties with respect to pH optima (pH5.0-5.5), oxygen requirement (0.6-0.7 mol of O(2) consumed/mol of ether degraded), inhibitors and reaction products. An unstable product breaks down to C(8) and C(9) carbonyl fragments. Both systems are inhibited by low concentrations of antioxidants (e.g. 5mum-butylated hydroxytoluene) and some chelating agents (e.g. 5mum-diethyldithio-carbamate). The model system is strongly inhibited by metal ions, particularly Cu(2+) and Fe(3+), at 20mum. Hydrogen peroxide and haemoproteins do not substitute for the enzyme or Fe(2+) ions but the non-haem iron protein, ferredoxin, does catalyse the degradation.

Antimetabolites↗
PubMed1988

Prostaglandin precursor fatty acids in cirrhosis with ascites: effect of linoleic acid infusion in functional renal failure.

1. Functional renal failure (FRF) in cirrhosis with ascites could be related to an inappropriately low renal prostaglandin (PG) production. To investigate whether the impaired renal PG synthesis in these patients is related to a PG precursor fatty acid deficiency, serum levels of linoleic and arachidonic acids and the urinary excretion of PGE2, 6-keto-PGF1 alpha and thromboxane B2 (TxB2) were measured in 10 normal subjects, 17 non-azotaemic cirrhotic patients with ascites and 10 cirrhotic patients with ascites and FRF. 2. Serum linoleic acid levels were similar in the three groups studied. Both groups of cirrhotic patients showed lower arachidonic acid levels than normal subjects; however, non-azotaemic cirrhotic patients and patients with FRF did not differ in relation to serum arachidonic acid. 3. Non-azotaemic cirrhotic patients had higher urinary PGE2, 6-keto-PGF1 alpha and TxB2 excretion than normal subjects and cirrhotic patients with FRF. Patients with FRF showed similar urinary PGE2 and TxB2 and lower urinary 6-keto-PGF1 alpha than normal subjects. In all cirrhotic patients no significant correlation was found between serum linoleic and arachidonic acid levels and urinary PGs. 4. In seven patients with FRF an acute intravenous infusion of linoleic acid induced a marked increase in serum levels of this fatty acid. However, no increase in serum arachidonic acid levels and urinary PG excretion and no improvement in renal function was observed. 5. This study suggests that an arachidonic acid deficiency is present in cirrhotic patients with ascites but that this abnormality is not a major determinant of renal function and PG production in these patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2001

Vaccenic acid feeding increases tissue levels of conjugated linoleic acid and suppresses development of premalignant lesions in rat mammary gland.

The objective of this report was to determine whether vaccenic acid (t11-18:1) is converted efficiently to conjugated linoleic acid (c9,t11-18:2, CLA) in rats via the delta 9-desaturase reaction and, if so, whether vaccenic acid could substitute for CLA as an anticancer agent. In Study 1, rats were fed 1%, 2%, or 3% vaccenic acid in their diet, and tissue levels of CLA and CLA metabolites were determined in liver and mammary gland. In general, concentrations of CLA and CLA metabolites increased proportionately with an increase in vaccenic acid intake, at least up to the 2% dose level. Beyond this dose, there was clearly a plateauing effect. Thus vaccenic acid concentration increased from an undetectable level in the control to 78.5 nmol/mg lipid in the liver of rats fed a 2% vaccenic acid diet. This was accompanied by an increase in CLA from 2.3 to 33.6 nmol/mg lipid. These changes were also mirrored in the mammary gland, where increases in vaccenic acid (from 27.5 to 163.2 nmol/mg lipid) and CLA (from 17.8 to 108.9 nmol/mg lipid) were similarly observed. Vaccenic acid at 2% produced a CLA concentration in the mammary gland that was historically associated with a positive response in tumor inhibition based on our past experience. This provided the basis for selecting 2% vaccenic acid in Study 2, which was designed to evaluate its efficacy in blocking the development of premalignant lesions in the rat mammary gland. In this experiment, formation of histologically identifiable pathology due to intraductal proliferation of terminal end bud cells of mammary epithelium was used as the end point of analysis at 6 wk after carcinogen administration. Treatment with vaccenic acid reduced the total number of these premalignant lesions by approximately 50%. We hypothesize that the anticancer response to vaccenic acid is likely to be mediated by its endogenous conversion to CLA via delta 9-desaturase.

8,11,14-Eicosatrienoic Acid↗
PubMed1985

Platelet fatty acid composition in relation to fatty acid composition in plasma and to serum lipoprotein lipids in healthy subjects with special reference to the linoleic acid pathway.

The fatty acid composition in platelet phospholipids and in the plasma lipid esters as well as the serum lipoprotein lipid concentrations were determined in 67 healthy male subjects in order to establish the relationships between blood lipids and platelets. A positive correlation was found between the concentrations of the triglyceride rich serum lipoprotein lipids and the relative percentage of saturated and monounsaturated fatty acids in plasma. The correlations were also positive between the serum high density lipoprotein-cholesterol concentration and the relative content of linoleic acid in the plasma cholesterol esters and phospholipids. Negative correlations were found between the relative percentage of saturated and monounsaturated fatty acids in the plasma lipid esters versus linoleic acid in plasma and in the platelets. On the other hand there were positive correlations between linoleic acid in the plasma lipid esters and in the platelet phospholipids. These results indicate a direct dietary influence on the platelet phospholipid fatty acid composition. The correlations between the fatty acids of the n-6 series within plasma and platelets as well as between plasma and platelets indicate that a high linoleic acid content is not associated with an increased arachidonic acid concentration. The results also indicate that the limiting metabolic step in the conversion of linoleic acid into arachidonic acid may be located at different levels in plasma and in the platelets.

Adult↗
PubMed1999

Metabolism of 13C-labeled linoleic acid in newborn infants during the first week of life.

Linoleic acid metabolism was studied during the first week of life in 10 breast-fed, full-term infants. Uniformly 13C-labeled linoleic acid (1 mg/kg body weight) was given orally. The 13C content was determined in expired CO2 over 6 h and in plasma phospholipid fatty acids over 3 d. Total CO2 production determined by indirect calorimetry was 16.7 +/- 10.6 mL/min (mean +/- SE). Over 6 h 7.4 +/- 0.6% of the ingested 13C-labeled linoleic acid was oxidized to CO2. Plasma phospholipid linoleic acid showed maximal 13C enrichment 24 h after tracer application (delta over baseline 178 +/- 24/1000). Enrichment of dihomo-gamma-linolenic acid increased from d 2 to d 5 of life (p < 0.002), with delta over baseline values of 2.1 +/- 0.5/1000 at 24 h, 3.7 +/- 10.9/1000 at 48 h, and 4.4 +/- 1.0/1000 at 72 h. 13C content of arachidonic acid tended to increase insignificantly. Areas under the curve of plasma tracer concentration over time were calculated for plasma n-6 phospholipid fatty acids. Percentages of total areas under the curve of the investigated n-6 fatty acids were 97.3 +/- 0.8% for linoleic acid, 1.5 +/- 0.6% for dihomo-gamma-linolenic acid, and 1.2 +/- 0.6% for arachidonic acid. The proportion of linoleic acid oxidized to CO2 did not correlate with the estimated conversion to long-chain polyunsaturated metabolites. Breast-fed newborn infants synthesize n-6 long-chain polyunsaturated fatty acids already during the first week of life, but the contribution of endogenous synthesis to the total plasma long-chain polyunsaturated pool is small. A major portion of dihomo-gamma-linolenic acid is converted to arachidonic acid.

8,11,14-Eicosatrienoic Acid↗
PubMed1994

Conjugated linoleic acid and atherosclerosis in rabbits.

Conjugated linoleic acid (CLA) consists of a series of positional and geometric dienoic isomers of linoleic acid that occur naturally in foods. CLA exhibits antioxidant activity in vitro and in vivo. To assess the effect of CLA on atherosclerosis, 12 rabbits were fed a semi-synthetic diet containing 14% fat and 0.1% cholesterol for 22 weeks. For 6 of these rabbits, the diet was augmented with CLA (0.5 g CLA/rabbit per day). Blood samples were taken monthly for lipid analysis. By 12 weeks total and LDL cholesterol and triglycerides were markedly lower in the CLA-fed group. Interestingly, the LDL cholesterol to HDL cholesterol ratio and total cholesterol to HDL cholesterol ratio were significantly reduced in CLA-fed rabbits. Examination of the aortas of CLA-fed rabbits showed less atherosclerosis.

Animals↗
PubMed2000

Linoleic acid and oleic acid increase the endothelin-1 binding and action in cultured rat aortic smooth muscle cells.

An increase in circulating non-esterified fatty acids (NEFA) has been observed in patients with poorly controlled diabetes mellitus. To investigate whether fatty acids will affect the endothelin-1 (ET-1) receptor and thus contribute to the acceleration of atherosclerosis in diabetic patients, cultured rat aortic smooth muscle cells (SMC) were maintained in media containing higher (similar to those in diabetic patients) concentrations of oleic acid (OA) or linoleic acid (LA). The ET-1 binding and ET-1-stimulated thymidine uptake were then examined. We found that cells treated with OA (500 micromol/L) or LA (250 micromol/L) showed a significant increase in ET-1 receptor amount as demonstrated by Scatchard analysis (Bmax: 7.40 +/- 1.04 v 2.71 +/- 0.54 fmol/mg and 5.00 +/- 1.00 v 3.32 +/- 0.70 fmol/mg, respectively). No change in binding affinity was found. Moreover, both the basal and ET-1-stimulated thymidine uptake were enhanced by treatment with either LA (basal, 11,367 +/- 4,117 cpm/mg; LA, 13,933 +/- 4,003 cpm/mg; ET-1 (10(-8)), 16,931 +/- 4,412 cpm/mg; LA +/- ET-1 (10(-8)), 28,855 +/- 5,217 cpm/mg) or OA (basal, 4,912 +/- 1,193 cpm/mg, OA, 8,027 +/- 1,318 cpm/mg; ET-1 (10(-8)) 9,947 +/- 2,520 cpm/mg; OA + ET-1 (10(-8)), 16,761 +/- 1,740 cpm/mg). This enhancement in thymidine uptake was associated with an increase in cell number. Because ET-1 and its receptor are involved in atherogenesis, our findings suggested that increase in circulating NEFA may contribute to the acceleration of atherosclerosis in diabetic patients. Further studies to confirm its role in the vascular wall are warranted.

Animals↗