Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “LINOLEIC ACID”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 415 records · Page 23Linked to original sources

Safflower oil consumption does not increase plasma conjugated linoleic acid concentrations in humans.

Conjugated linoleic acid (CLA) is a mixture of positional and geometric isomers of linoleic acid (LA) with conjugated double bonds. CLA has anticarcinogenic properties and has been identified in human tissues, dairy products, meats, and certain vegetable oils. A variety of animal products are good sources of CLA, but plant oils contain much less. However, plant oils are a rich source of LA, which may be isomerized to CLA by intestinal microorganisms in humans. To investigate the effect of triacylglycerol-esterified LA consumption on plasma concentrations of esterified CLA in total lipids, a dietary intervention (6 wk) was conducted with six men and six women. During the intervention period a salad dressing containing 21 g safflower oil providing 16 g LA/d was added to the subjects' daily diets. Three-day diet records and fasting blood were obtained initially and during dietary and postdietary intervention periods. Although LA intake increased significantly during the dietary intervention, plasma CLA concentrations were not affected. Plasma total cholesterol and LDL-cholesterol concentrations were significantly lower after addition of safflower oil to the diet. In summary, consumption of triacylglycerol-esterified LA in safflower oil did not increase plasma concentrations of esterified CLA in total lipids.

Adult↗

[Effect of dietary fats on serum and aortic lipid levels of mice fed a high-cholesterol diet: a distinct correlation between linoleic acid intake and the lipid changes].

The effects of dietary linoleic acid on serum lipids, lipid peroxides and aortic cholesterol were studied in mice fed a purified diet enriched with 5% cholesterol for a period of 14 weeks. The diet was supplemented with 10% coconut oil (Group I), lard (Group II), corn oil (Group III) or linoleic acid (Group IV) to give various levels of linoleic acid. After 4 to 12 weeks, the increment of serum total cholesterol was retained in the following order: group IV greater than III greater than II greater than I, which was the same order as the linoleic acid content in the diet. At week 14, the levels of serum free and esterified cholesterol, HDL-cholesterol, triglycerides and phospholipids were highest in group IV and lowest in group I. The serum lipid peroxide level was higher in the order of group IV greater than III greater than II greater than I. The ester ratio of cholesterol, the atherogenic index and LCAT activity were not significantly different among the four groups. Gallstone formation was markedly observed with higher dietary linoleic acid intake. Aortic cholesterol levels also increased in the same order as the dietary linoleic acid level: group IV greater than III greater than II greater than I. There were significant positive correlations between the aortic cholesterol level and all the serum lipid levels, and also the lipid peroxide level. All these findings indicate that under hypercholesterolemic conditions, excess dietary linoleic acid can increase serum lipids and lipid peroxide levels, resulting in lipid deposition in the aorta.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

C18:1, C18:2 and C18:3 trans and cis fatty acid isomers including conjugated cis delta 9, trans delta 11 linoleic acid (CLA) as well as total fat composition of German human milk lipids.

In particular with respect to infant nutrition knowledge of the current contents of trans fatty acids (TFA) and of conjugated linoleic acid (CLA in human milk lipids is of interest. After pre-separation by Ag-TLC 11 trans-C18:1 isomers could be quantified by GC with a mean total content of 2.40 +/- 0.60 wt% in samples from 40 German women. For the positional isomers t4, t5, t6-8, t9, t10, t11, t12, t13, t14, t15 and t16 contents of 0.02, 0.02, 0.21, 0.37, 0.32, 0.68, 0.23, 0.15, 0.18, 0.09 and 0.14 wt% were established, with vaccenic acid being the predominant isomer. Further, small trans-C14:1 and trans-C16:1 contents of 0.08% and 0.15% on average were found. As the trans-C18:1 isomers also the trans-C16:1 isomers of human milk lipids could for the first time be baseline-resolved by GC to a great extent. Moreover, besides a mean CLA (c9,t11) content of 0.40 +/- 0.09% further 6 cis/trans isomers of linoleic acid with a total content of 1.07 +/- 0.56% on average (w/o CLA) were determined. Further, 4 trans isomers of alpha-linolenic acid could be baseline-resolved exhibiting a total content of 0.11%. Altogether German human milk lipids on average were found to contain 3.81 +/- 0.97% TFA with a range of 2.38-6.03%. Direct connections between the dietary intake of trans-C18:1 isomers and the composition of human milk lipids could be established. The major fatty acids exhibited the following contents (wt%): C4: 0.16, C6: 0.18, C8: 0.06, C10: 0.58, C12: 3.12, C14: 6.43, C16: 25.28, C18: 7.41, C18: 1 (total): 33.67, C18: 2 (total): 10.63 and alpha-C18: 3:0.87.

Adult↗

Effects of dietary linoleic acid on blood pressure and renal function in subtotally nephrectomized rats.

The effect of a high linoleic acid diet on blood pressure, renal function, and urinary prostaglandin excretion was studied in rats with decreased renal mass. Subtotally nephrectomized (5/6 nephrectomy) male rats received either a 15% linoleic acid (high linoleic acid, HLA) diet containing 20% safflower oil or a 0.28% linoleic acid (low linoleic acid, LLA) diet containing 20% coconut oil. Sham-operated rats were also placed on either HLA or LLA diet. The subtotal nephrectomized rats developed similar degrees of hypertension during the first 3 weeks after subtotal nephrectomy. However, 4 weeks after subtotal nephrectomy, the rats on HLA diet had significantly lower blood pressure than the rats on LLA diet [HLA 152 +/- 3 (mean +/- SE) mm Hg versus LLA 171 +/- 3 mm Hg]. This difference persisted until termination of the experiment at 7 weeks after subtotal nephrectomy (HLA 159 +/- 7 mm Hg versus LLA 192 +/- 6 mm Hg). The GFR measured 7 weeks after subtotal nephrectomy was significantly lower in both of the subtotally nephrectomized groups. However, the HLA subtotal nephrectomized rats had significantly higher GFR than the LLA-treated rats (HLA 0.23 +/- 0.05 ml/min 100 g versus LLA 0.12 +/- 0.02 ml/min/100 g, P less than 0.05). There was no difference in the GFR or blood pressure in the sham-operated rats treated with HLA or LLA diet. PGE2 excretion was lower in the two groups of subnephrectomized rats, but there was no difference between the HLA and LLA treated rats. Urinary 6-ketoPGF1 alpha was not decreased by subtotal nephrectomy and there was no difference between the dietary groups. However, TXB2 excretion was higher in the groups with subtotal nephrectomy, but there was no difference between the two dietary groups. In conclusion, the HLA diet attenuates the rise in blood pressure after subtotal nephrectomy in the rat and preserves renal function. There was no difference in urinary excretion of PGE2, 6-keto-PFG1 alpha, or thromboxane B2 between the two dietary groups.

6-Ketoprostaglandin F1 alpha↗

Effect of dietary fats on linoleic acid metabolism. A radiolabel study in rats.

Effects on the linoleic acid metabolism in vivo of three dietary fats, rich in either oleic acid, trans fatty acids or alpha-linolenic acid, and all with the same linoleic acid content, were investigated in male Wistar rats. After 6 weeks of feeding, the rats were intubated with [1-14C]linoleic acid and [3H]oleic acid. The incorporation of these radiolabels into liver, heart and serum was investigated 2, 4, 8, 24 and 48 h after intubation. The amount of 14C-labelled arachidonic acid incorporated into the liver phospholipid of the group fed the oleic acid-rich diet was significantly higher than that of the other groups. However, compared to the trans fatty acids-containing diet, the oleic acid-rich diet induced only a slightly higher arachidonic acid level in the phospholipid fraction of the tissues as determined by GLC. Dietary alpha-linolenic acid more than halved the arachidonic acid levels. Our results do not support the hypothesis that the delta 6-desaturase system actually determines the polyunsaturated fatty acid levels in tissue lipids by regulating the amount of polyunsaturated fatty acids (e.g., arachidonic acid) synthesized. The biosynthesis of polyunsaturated fatty acids only is not sufficient to explain the complicated changes in fatty acid compositions as observed after feeding different dietary fats.

Animals↗

Stereochemistry of oxygenation of linoleic acid catalyzed by prostaglandin-endoperoxide H synthase-2.

Linoleic acid was incubated with prostaglandin-endoperoxide H synthase-2 (PGHS-2) from ovine placenta. A product consisting of regio- and stereoisomeric hydroxyoctadecadienoic (HOD) acids was obtained. Analysis by straight-phase high-performance liquid chromatography followed by chiral-phase high-performance liquid chromatography demonstrated that linoleic acid was preferentially oxygenated at C-9 to produce the following mixture of HODs: 9(R)-HOD (52%), 9(S)-HOD (11%), 13(R)-HOD (2%), and 13(S)-HOD (35%). As a comparison, linoleic acid was incubated with microsomal prostaglandin-endoperoxide H synthase-1 (PGHS-1) from ovine vesicular gland. This resulted in a product having the following composition: 9(R)-HOD (73%), 9(S)-HOD (9%), 13(R)-HOD (1%), and 13(S)-HOD (17%). The stereochemistry of the hydrogen which was removed from C-11 during the conversion of linoleic acid into hydroxy acids in the presence of PGHS-1 or PGHS-2 was determined by incubation of [(11R)-2H]- and [(11S)-2H]linoleic acids followed by mass spectrometric analysis of the isotope contents of the individual hydroxy acid isomers. Both enzymes were found to catalyze oxygenations which involved stereospecific removal of the (11S) hydrogen and retention of the (11R) hydrogen. The major hydroxy acids, i.e., 9(R)-HOD and 13(S)-HOD, were formed from linoleic acid in reactions which involved antarafacial hydrogen abstraction and oxygen insertion. It is concluded that the initial steps of the PGHS-2- and PGHS-1-catalyzed oxygenations proceed with identical stereochemistry and involve stereospecific removal of the pro-S hydrogen from the omega 8-methylene group of the substrate.

Animals↗

Prostaglandin formation in man during intake of different amounts of linoleic acid in formula diets.

Prostaglandin formation in healthy female volunteers was investigated during intake of different amounts of linoleic acid in liquid formula diets (LFD). The average amounts of the metabolites convertible to tetranorprostanedioic acid (TNPDA) were 123 +/- 5.2 (x +/- SEM), 175 +/- 7.0 and 352 +/- 10.8 microgram/day, during 2-week periods with a linoleic acid supply of 0, 4 or 20% of energy, respectively. The day-by-day variations in prostaglandin formation were less than the changes observed due to different amounts of linoleic acid. High linoleic acid intake was followed by an increase of TNPDA in the urine after 3-4 days, which was more pronounced when the linoleic acid intake during the period before had been low. In all persons, the highest amount of TNPDA, 411 +/- 13.2 microgram/day, was found between days 5 and 10 of high linoleic acid intake. From day 11 through day 14 an average of 372 +/- 14.3 microgram/day was found and the values were lower in 5 of 6 persons as compared to the values found between days 5 and 10. At the end of the experiment with LFD providing a linoleic acid supply of 0, 4 or 20% of energy, the percentage of cholesteryl linoleate in plasma increased (35 +/- 1.8, 48 +/- 1.0, 63 +/- 0.6) while those of cholesterylarachidonate decreased (14 +/- 1.0, 10 +/- 0.6, 8 +/- 0.6). During the periods without linoleic acid intake the TNPDA excretion was lowest in all persons. A reduction in linoleic acid supply resulted in a decrease of urinary TNPDA within 1 day.

Adult↗

Dietary conjugated linoleic acid and body composition.

Conjugated linoleic acid (CLA) is a group of positional and geometric isomers of conjugated dienoic derivatives of linoleic acid. The major dietary source of CLA for humans is ruminant meats, such as beef and lamb, and dairy products, such as milk and cheese. The major isomer of CLA in natural food is cis-9,trans-11 (c9,t11). The commercial preparations contain approximately equal amounts of c9,t11 and trans-10,cis-12 (t10,c12) isomers. Studies have shown that CLA, specifically the t10,c12-isomer, can reduce fat tissue deposition and body lipid content but appears to induce insulin resistance and fatty liver and spleen in various animals. A few human studies suggest that CLA supplementation has no effect on body weight and could reduce body fat to a much lesser extent than in animals. To draw conclusions on this form of dietary supplementation and to ultimately make appropriate recommendations, further human studies are required. The postulated antiobesity mechanisms of CLA include decreased energy and food intakes, decreased lipogenesis, and increased energy expenditure, lipolysis, and fat oxidation. This review addresses recent studies of the effects of CLA on lipid metabolism, fat deposition, and body composition in both animals and humans as well as the mechanisms surrounding these effects.

Adipose Tissue↗

Influence of linoleic acid content of the diet on arterial pressure of salt loaded rats. I. Effects on prostaglandin metabolism and sympathetic nervous system.

1. Compared with linoleic acid rich and pellet diet linoleic acid free diet causes an increase in blood pressure in salt loaded rats. The blood pressure increasing effect of linoleic acid poor diet could not be augmented by linoleic acid free diet. 2. The blood pressure was increased by indomethacin in linoleic acid rich and pellet fed rats. In linoleic acid free fed animals indomethacin shows only a brief augmentation of blood pressure. 3. Prostaglandin (PG) biosynthesis was decreased in isolated kidneys and aorta but increased in the kidney medulla homogenate after a four-week linoleic acid free diet. 4.. Chemical sympathectomy by intracerebroventricular injections of 6-hydroxydopamine abolished the blood pressure increasing effect of linoleic acid free diet. We postulate that changes in the PG metabolism and in the activity of sympathetic nervous system are causes for the elevated blood pressure of linoleic acid free fed salt loaded rats and we conclude that the function of the cardiovascular system is influenced favourably by a linoleic acid rich diet.

Animals↗

Linoleic acid metabolism and prostaglandin production by cultured bovine pulmonary artery endothelial cells.

When bovine pulmonary artery endothelial cells are cultured in a medium supplemented with linoleic acid, their capacity to produce prostacyclin (PGI2) is reduced by about 60%. This reduction occurs when PGI2 formation is stimulated by the addition of either the calcium ionophore A23187 or arachidonic acid. In addition, supplementation with linoleic acid reduced the production of prostaglandin E2 and F2 alpha from 1-14C-arachidonic acid by more than 50%. The capacity of cultured bovine pulmonary vein and aortic endothelial cells to convert extracellular arachidonic acid into PGI2 also was reduced by about 50% when the growth medium was supplemented with linoleic acid. Although bovine pulmonary artery endothelial cells incorporated large amounts of 1-14C-linoleic acid into cellular phospholipids and triglycerides, a maximum of only 2.3% of the radioactivity was converted to arachidonic acid in 24 hours. The most prevalent radioactive metabolite was eicosadienoic acid, the elongation product of linoleic acid. As compared with linoleic acid, the bovine endothelial cells incorporated 30% more 1-14C-arachidonic acid into phospholipids and 60% more into triglycerides. When the growth medium was supplemented with linoleic acid, the percentage of this fatty acid in cellular lipids increased 3- to 4.5-fold and eicosadienoic acid accumulated, accounting for up to 9% of the cellular fatty acids. This increase was accompanied by a 30% to 45% reduction in arachidonic acid. These findings, together with our previous results with human umbilical vein endothelium, suggest that an inability to convert large amounts of linoleic to arachidonic acid and a suppressive effect of linoleic acid enrichment on prostaglandin production may be general properties of endothelial cells.

Animals↗

Influence of different supplements of N-3 polyunsaturated fatty acids on blood and tissue lipids in rats receiving high intakes of linoleic acid.

The influence of a supplement of linseed oil (LO), rich in linoleic acid (C18:3,n-3), was compared with one of fish oil (MaxEPA) rich in eicosapentaenoic acid (C20:5,n-3) and docosahexaenoic acid (22:6,n-3) on blood and tissue lipids in weanling rats receiving a high intake of linoleic acid. Both the LO and the MaxEPA supplement decreased plasma cholesterol concentrations. The MaxEPA supplement but not the linseed oil supplement also decreased the concentrations of plasma triglycerides and HDL cholesterol. The proportion of C20:5,n-3 was markedly increased in the platelet and erythrocyte lipids by the MaxEPA supplement but not in tissue lipids. However, the increase in the proportion of C20:5,n-3 in the platelet was small compared with other studies. Both supplements led to an increase in the proportion of C22:6,n-3 in blood and tissue lipids but the MaxEPA supplement was more potent than the LO supplement. The most marked change was observed in the heart lipids. These changes were accompanied by reciprocal changes in the proportions of arachidonic, adrenic and docosapentaenoic acid.

Adipose Tissue↗

Neutrophils from pregnant women produce thromboxane and tumor necrosis factor-alpha in response to linoleic acid and oxidative stress.

OBJECTIVE: Preeclampsia is associated with oxidative stress, neutrophil activation, neutrophil infiltration into systemic vasculature, and elevated plasma levels of linoleic acid, the fatty acid precursor to arachidonic acid and its metabolite, thromboxane. In this study we evaluated whether linoleic acid under conditions of oxidative stress would stimulate neutrophil production of thromboxane and tumor necrosis factor-alpha. STUDY DESIGN: Neutrophils were isolated from 14 normal pregnant women. Western blot demonstrated cyclooxygenase-2 expression at 18 hours of incubation, so this incubation time was used for experiments. Neutrophils (2 x 10(6) cells/mL) were incubated in Dulbecco's modified Eagle's medium/F-12 with: (1) linoleic acid control; (2) an oxidizing solution enriched with linoleic acid; (3) oxidizing solution enriched with linoleic acid plus indomethacin; (4) oxidizing solution enriched with linoleic acid plus aspirin; (5) oxidizing solution enriched with linoleic acid plus NS-398, a specific inhibitor of cyclooxygenase-2; or (6) oxidizing solution enriched with linoleic acid plus pinane thromboxane, a thromboxane synthase inhibitor and receptor blocker. RESULTS: Oxidizing solution enriched with linoleic acid significantly increased oxidative stress in neutrophils. Compared with linoleic acid, oxidizing solution enriched with linoleic acid significantly increased neutrophil production of thromboxane and tumor necrosis factor-alpha. Indomethacin and aspirin inhibited oxidizing solution enriched with linoleic acid stimulation of thromboxane, but NS-398 was equally effective implicating cyclooxygenase-2 in the thromboxane response. Indomethacin inhibited oxidizing solution enriched with linoleic acid stimulation of tumor necrosis factor-alpha, but so did pinane thromboxane implicating thromboxane in the tumor necrosis factor-alpha response. CONCLUSIONS: These data demonstrate that exposure of neutrophils from normal pregnant women to conditions present in preeclamptic women results in neutrophil activation with release of thromboxane and tumor necrosis factor-alpha. Newly synthesized thromboxane is cyclooxygenase-2 dependent and plays a role in the tumor necrosis factor-alpha response. Our data suggest a mechanism for maternal vasoconstriction and vascular inflammation in preeclampsia because activated, thromboxane-secreting neutrophils migrate across endothelium into the microenvironment of the vasculature in which they could promote vasoconstriction, whereas release of tumor necrosis factor-alpha could cause vascular inflammation.

Blotting, Western↗

Injury to cultured endothelial cells from human umbilical vein by linoleic acid hydroperoxide.

The effect of linoleic acid hydroperoxide on cultured endothelial cells from human umbilical vein was examined morphologically. Incubation of the cells with a low concentration (0.5 nmol/ml) of linoleic acid hydroperoxide for 3 h caused a slight decrease in electron density of the mitochondrial matrix. Upon an increase of the concentration to 1.0 nmol/ml, the damage became more pronounced, and enlargement and dilatation of the rough-surfaced endoplasmic reticulum were observed. At higher concentrations (5 and 7.5 nmol/ml), dilatation of the rough-surfaced endoplasmic reticulum became further pronounced, and many vacuoles were observed in the cells.

Cells, Cultured↗

Linoleic acid content in adipose tissue and coronary heart disease.

The possibility of an inverse relation between essential fatty acids in adipose tissue, in particular linoleic acid, and mortality from coronary heart disease was studied by a cross sectional survey of random population samples of apparently healthy men aged 40-49 from four European regions with differing mortality from coronary heart disease. The proportion of linoleic acid in adipose tissue was lowest in men from north Karelia, Finland, where mortality from coronary heart disease is highest, and highest in men from Italy, where mortality is lowest, with intermediate proportions in men from Scotland and south west Finland. Similar gradients were observed for the desaturation and elongation products dihomo-gamma-linolenic and arachidonic acid. The proportion of saturated fatty acids in adipose tissue was highest in Finland, intermediate in Scotland, and lowest in Italy. Italian men also had the highest proportion of oleate in their adipose tissue and the lowest proportion of myristoleate and palmitoleate. Finnish men were more obese and had a higher blood pressure. Serum cholesterol concentration was higher in north Karelia and south west Finland than in Scotland or Italy. High density lipoprotein (HDL) cholesterol concentrations reflected the regional differences in serum cholesterol, being higher in Finland and lower in Italy. The ratios of HDL cholesterol to total cholesterol, however, did not differ. The regional differences in linoleic acid in adipose tissue remained highly significant when the observed differences in other known risk factors for coronary heart disease among the four areas were taken into account by multivariate analysis. The gradients in proportions of polyunsaturated fatty acids probably reflect differences in dietary intake of linoleic acid.

Adipose Tissue↗

The role of superoxide in xanthine oxidase-induced autooxidation of linoleic acid.

The effect of hydroxyperoxyoctadecadienoic acid, e.g. 13-hydroperoxy-cis,9,trans-11-octadecadienoic acid, on the autooxidation of linoleic acid induced by superoxide radical was examined in a system containing xanthine oxidase, acetaldehyde, and diethylenetriaminepentaacetic acid dissolved in an aqueous phosphate buffer containing 10% ethanol. The superoxide radical is required for autooxidation, as shown by essentially complete inhibition on the addition of superoxide dismutase. Pure linoleic acid was not readily oxidized, but the addition of lipid hydroperoxide markedly stimulated the autooxidation. Addition of 2.8 microM FeCl3 did not produce an increase in the rate of xanthine oxidase-induced autooxidation. Spontaneous autooxidation, a process slower than xanthine oxidase-induced autooxidation, was detectable on the time scale of these observations but was slower than the xanthine oxidase-induced autooxidation. Initiation of linoleic acid autooxidation is postulated to result from a reaction between superoxide and lipid hydroperoxide. The nature of this reaction is uncertain, but it does not appear to depend on iron catalysis.

Animals↗

Oxygenation of linolenic and linoleic acid to novel vicinal dihydroxy acids by hepatic microsomes of the rabbit.

[14C] Linolenic acid (18: omega 3) and [14C] linoleic acid (18:2 omega 6) were incubated with hepatic microsomes of the rabbit in the presence of NADPH (1 Mm) for 15 min at 37 degrees C. The products were extracted and purified by high performance liquid chromatography. The major metabolites of linolenic and linoleic acid were identified by capillary gas chromatography mass spectrometry as 15,16-dihydroxy-9,12-octadecadienoic acid, 12,13-dihydroxy-9,15-octadecadienoic acid and 9,10-dihydroxy-12,15-octadecadienoic acid and as 12,13-dihydroxy-9-octadecaenoic acid and 9,10-dihydroxy-12-octadecaenoic acid, respectively. The results were confirmed by comparison with mass spectra of the authentic compounds. These metabolites are presumably formed by cytochrome P-450 catalyzed epoxidation of the omega 3, omega 6 and omega 9 double bonds, followed by enzymatic hydrolysis to 1,2-diols. The ratio of omega 3, omega 6 and omega 9 oxygenated metabolites of linolenic acid was approximately 2:1:1 and the ratio of the omega 6 and omega 9 metabolites of linoleic acid was 2:1, indicating that the double bond closest the omega end is most easily oxygenated.

Animals↗

The metabolic conversion of 9,11,13-eleostearic acid (18:3) to 9,11-conjugated linoleic acid (18:2) in the rat.

The presence of a significant amount of 9,11-conjugated linoleic acid (CLA, 9,11-18:2) was confirmed in the liver and plasma lipids of rats fed a 1% (w/w % of diet) eleostearic acid (ESA, 9,11,13-18:3) diet for 4 wk. The chemical structure of the 9,11-CLA apparent in the tissue lipids was identified by gas chromatography-electron impact mass spectrometry after its conversion to a 4,4-dimethyloxazoline derivative. The concentration of CLA in the total fatty acids of the liver and plasma lipids reached to about 1%, for each in the CLA-supplemented rats, while reaching 3.2% and 2.5%, respectively, in the ESA-supplemented rats. The results suggest that alpha-ESA is metabolized partially to CLA via a delta 13-saturation reaction in the rat. Some biological activities observed in alpha-ESA-fed animals may be ascribed also to CLA that is formed from ESA in the body.

Animals↗

The enrichment of a ruminal bacterium (Megasphaera elsdenii YJ-4) that produces the trans-10, cis-12 isomer of conjugated linoleic acid.

AIMS: To isolate predominant ruminal bacteria that produce trans-10, cis-12 conjugated linoleic acid (CLA) from linoleic acid (LA). METHODS AND RESULTS: Mixed bacteria from ruminal contents of a cow fed grain were enriched with DL-lactate and trypticase. They produced more trans-10, cis-12 CLA than those that were not enriched (7 vs 2 microg mg protein(-1), P < 0.05). Enrichments had an abundance of large cocci that produced trans-10, cis-12 CLA from LA. Strain YJ-4 produced the most trans-10, cis-12 CLA (approx. 7 microg mg protein(-1)) and 16S rDNA sequencing indicated that YJ-4 was a strain of Megasphaera elsdenii. Megasphaera elsdenii T81 produced approx. 4 microg trans-10, cis-12 CLA mg protein(-1) while strains B159, AW106 and JL1 produced < 0.5 microg mg protein(-1). The trans-10, cis-12 CLA production of YJ-4 was first order with respect to cell concentration (0-800 microg protein ml(-1)), but kinetics were not first order with respect to substrate concentration. CONCLUSIONS: Some M. elsdenii strains produce significant amounts of trans-10, cis-12 CLA. SIGNIFICANCE AND IMPACT OF THE STUDY: Trans-10, cis-12 CLA appears to cause milk fat depression in cattle fed diets supplemented with grain and polyunsaturated fatty acids, but predominant ruminal bacteria that produced trans-10, cis-12 CLA from LA had not previously been isolated.

Animals↗