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PubMed2006

Fatty acid composition of liver, adipose tissue, spleen, and heart of mice fed diets containing t10, c12-, and c9, t11-conjugated linoleic acid.

Conjugated linoleic acid (CLA) isomers have unique effects on tissue lipids. Here we investigated the influence of individual CLA isomers on the lipid weight and fatty acid composition of lipid metabolizing (i.e. liver and retroperitoneal adipose) and lipid sensitive (i.e. spleen and heart) tissues. Female mice (8 week old; n=6/group) were fed either a control or one of the two CLA isomer supplemented (0.5%) diets for 8 weeks. The cis-9, trans-11-CLA diet reduced the 18:1n-9 wt% by 20-50% in liver, adipose tissue, and spleen, reduced the spleen n-3 polyunsaturated fatty acid (PUFA) by 90%, and increased the n-6 PUFA wt% by 20-50% in all tissues except heart. The trans-10, cis-12-CLA reduced both the n-6 and n-3 PUFA wt% in liver (>50%), reduced the heart n-3 PUFA wt% by 25%, and increased the wt% of spleen n-3 PUFA by 700%. The functional consequences of such changes in tissue fatty acid composition need to be investigated.

Adipose Tissue↗
PubMed2004

Differential inhibition of fatty acid transport in tissue-isolated steroid receptor negative human breast cancer xenografts perfused in situ with isomers of conjugated linoleic acid.

In established rodent tumors and human cancer cell lines, conjugated dienoic isomers of linoleic acid (CLA) suppress the growth-stimulating effects of linoleic acid (LA) and its metabolism to the mitogenic agent, 13-hydroxyoctadecadienoic acid (13-HODE). Here, we compared the effects of three CLA isomers on LA uptake and metabolism, and growth in human breast xenografts perfused in situ in female nude rats. The results demonstrated that two CLA isomers [10t, 12c-CLA>9t, 11t-CLA] caused a dose-dependent inhibition of LA uptake, cAMP content, 13-HODE formation, Erk 1/2 activity, and [(3)H]thymidine incorporation into tumor DNA; 9c, 11t-CLA showed no effect. The inhibitory effect is reversible with either pertussis toxin (PTX) or 8-Br-cAMP suggesting that CLA isomers differentially inhibit LA uptake and metabolism and cell proliferation in human breast cancer in vivo via a receptor-mediated, PTX-sensitive pathway.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed2006

Microbially safe utilization of non-inactivated oats (Avena sativa L.) for production of conjugated linoleic acid.

A microbially safe process for the enrichment of conjugated linoleic acid (CLA) in oats was developed. The process consists of hydrolysis of oat lipids by non-inactivated oat flour, followed by propionibacterium-catalyzed isomerization of the resulting free linoleic acid to CLA. The first stage was performed at water activity (a(w)) 0.7, where hydrolysis of triacylglycerols progressed efficiently without growth of the indigenous microflora of flour. Thereafter, the flour was incubated as a 5% (w/v) aqueous, sterilized slurry with Propionibacterium freudenreichii ssp. shermanii. The amount of CLA produced in 20 h was 11.5 mg/g dry matter corresponding to 116 mg/g lipids or 0.57 mg/mL slurry. The oat flour had also the capability to hydrolyze exogenous oils at a(w) 0.7. Sunflower oil, added to increase linoleic acid content in triacylglycerols 2.7-fold, was hydrolyzed rapidly. Isomerization of this oil-supplemented flour as a 5% slurry gave final CLA content of 22.3 mg/g dry matter after 50 h of fermentation, corresponding to 118 mg/g lipids or 1.14 mg/mL slurry. Storage stability of CLA in fermented oat slurries at 4 degrees C was good.

Avena↗
PubMed1999

Stability of cyclopropane and conjugated linoleic acids during fatty acid quantification in lactic acid bacteria.

Seven methods commonly used for fatty acid analysis of microorganisms and foods were compared to establish the best for the analysis of lyophilized lactic acid bacteria. One of these methods involves fat extraction followed by methylation of fatty acids, while the other methods use a direct methylation of the samples, under different operating conditions (e.g., reaction temperature and time, reagents, and pH). Fatty acid methyl esters were identified by gas chromatography-mass spectrometry and quantified by on-column capillary gas chromatography. Two reliable methods for the analysis of fatty acids in bacteria were selected and further improved. They guarantee high recovery of classes of fragile fatty acids, such as cyclopropane and conjugated acids, and a high degree of methylation for all types of fatty acid esters. These two direct methylation methods have already been successfully applied to the analysis of fatty acids in foods. They represent a rapid and highly reliable alternative to classical time- and solvent-consuming methods and they give the fatty acid profile and the amount of each fatty acid. Using these methods, conjugated linoleic acids were identified and quantified in lactic acid bacteria.

Bacteria↗
PubMed1987

Conversion of linoleic acid and arachidonic acid by skin epidermal lipoxygenases.

Two different lipoxygenases have been identified in human and rat epidermis. One lipoxygenase has a (n-9)-specificity, converts arachidonic acid into 12-hydroxyeicosatetraenoic acid (12-HETE), and has been described by several investigators. Linoleic acid is not a substrate for this enzyme. The other lipoxygenase, with (n-6)-specificity, converts arachidonic acid into 15-HETE and linoleic acid into 13-hydroxyoctadecadienoic acid (13-HOD). Especially the latter lipoxygenase is thought to be involved in the regulation of the differentiation of the skin cells into a proper water-barrier layer. Linoleate is supposed to be the physiological substrate; this fatty acid is especially present in characteristic sphingolipids with unique structures.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1975

[Effects of linoleic acid hydroperoxide on the formation of lipid peroxide in the rat liver mitochondria].

An in vivo study was made on the effect of linoleic acid hydroperoxide on the formation of lipid peroxide in rat liver mitochondria, and results are as follows: There were no changes in contents of lipid peroxide and total sulfhydryl in rat liver mitochondria after daily administration of linoleic acid hydroperoxide (10 mg/kg, i.p.) for 3 or 7 days. Changes in the fatty acid composition in plasma and liver after i.p. administration of linoleic acid hydroperoxide for one week were not observed as compared to that of control animals. In addition, no appreciable change was found in the fatty acid composition of phosphatidylserine and phosphatidylinositol in liver mitochondria from rats treated with linoleic acid hydroperoxide. After treatment with linoleic acid hydroperoxide for 3 days, content of plasma triglycerides increased, but no effect was observed in liver triglycerides. However, plasma triglycerides returned to the control level and triglycerides in liver increased by treatment with linoleic acid hydroperoxide for one week. Free fatty acids decreased in plasma but not in the liver from rats treated with linoleic acid hydroperoxide for 3 or 7 days.

Animals↗
PubMed2002

The effect of dietary supplementation using isomeric blends of conjugated linoleic acid on lipid metabolism in healthy human subjects.

Conjugated linoleic acid (CLA) refers to a group of positional and geometric isomers of linoleic acid. Studies using animal models have shown that CLA reduces adiposity, improves plasma lipoprotein metabolism and insulin sensitivity and reduces arteriosclerosis. Whilst CLA may have therapeutic potential with regard to coronary artery disease risk factors in human subjects, there has been little investigation into its effects in human subjects. This current study investigated the effects of dietary supplementation using two isomeric blends of CLA on triacylglycerol (TAG)-rich lipoprotein metabolism and reverse cholesterol transport in human subjects and evaluates whether CLA modulated cardiovascular disease risk factors. Fifty-one normolipidaemic subjects participated in this randomised double-blind placebo-controlled intervention trial. Subjects were randomly assigned to receive 3 g cis-9,trans-11-trans-10,cis-12 isomeric blend (50 : 50) or a cis-9,trans-11-trans-10,cis-12 isomeric blend (80 : 20) CLA or linoleic acid (control)/d for 8 weeks. The 50 : 50 CLA isomer blend significantly reduced (P<or=0.005) fasting plasma TAG concentrations. The 80 : 20 CLA isomer blend significantly reduced (P<or=0.05) VLDL-cholesterol concentrations. CLA supplementation had no significant effect on LDL-cholesterol, HDL-lipid-protein composition or reverse cholesterol transport. CLA supplementation had no effect on body weight, plasma glucose and insulin concentrations. Fatty acid analysis revealed that the cis-9,trans-11 CLA isomer was incorporated into total plasma lipids following supplementation with both isomeric blends of CLA. The present study demonstrates that CLA supplementation significantly improves plasma TAG and VLDL metabolism in human subjects. The study confirms that some of the cardio-protective effects of CLA that were shown in animal studies are relevant to man.

Adult↗
PubMed2002

Dietary conjugated linoleic acid reduces body fat mass and affects gene expression of proteins regulating energy metabolism in mice.

ICR and C57BL/6J mice were fed experimental diets containing either a 2% fatty acid preparation rich in conjugated linoleic acid (CLA) or a preparation rich in linoleic acid and free of CLA for 21 days. CLA greatly decreased weights of white adipose tissue and interscapular brown adipose tissue in the two strains. CLA reduced mRNA levels of glucose transporter 4 (Glut 4) in white and brown adipose tissue of both strains. A CLA-dependent decrease in mRNA levels of peroxisome proliferator activated receptor (PPAR) gamma was seen in interscapular brown adipose tissue of both strains and in white adipose tissue of C57BL/6J but not ICR mice. Dietary CLA was found to cause a decrease in the mRNA levels of uncoupling protein (UCP) 1 in brown adipose tissue when the value was corrected for the expression of a house-keeping gene (beta-actin) in the two strains. Uncorrected values were, however, indistinguishable between the animals fed the CLA diet and CLA-free diet. UCP 3 expression in brown adipose tissue was much lower in mice fed the CLA diet than in those fed the control diet in both strains. In contrast, CLA greatly up-regulated the gene expression of UCP 2 in brown adipose tissue. Dietary CLA also increased UCP 2 mRNA level in skeletal muscle. It is apparent that dietary CLA decreases white and brown adipose tissue mass, accompanying changes in the gene expression of proteins regulating energy metabolism in white and brown adipose tissues, and skeletal muscle of mice.

Adipose Tissue↗
PubMed1989

Hypotriglyceridemic effect of dietary n - 3 fatty acids in rats fed low versus high levels of linoleic acid.

The effect of dietary alpha-linolenic acid (linseed oil) or eicosapentaenoic acid (fish oil) on serum and liver triacylglycerol levels in rats fed diets rich in saturated fatty acids (hydrogenated beef tallow) versus high in linoleic acid (safflower oil) was examined. Feeding fish oil with hydrogenated tallow lowered the serum triacylglycerol concentration while the combination of fish oil and safflower oil failed to do so. Inclusion of fish oil in the hydrogenated tallow diet lowered the triacylglycerol constant in level tissue whereas inclusion of linseed oil had no significant effect. Feeding of linseed oil or fish oil in the safflower oil diet resulted in lowering of the liver triacylglycerol levels. These results suggest that dietary fish oil may have greater hypotriglyceridemic effects in individuals/populations eating diets high in saturated fats compared with those consuming mainly polyunsaturated vegetable oils rich in n - 6 fatty acids.

Animals↗
PubMed1994

Effects of dietary linoleic acid on pancreatic carcinogenesis in rats and hamsters.

It has been suggested that linoleic acid (LA) is responsible for the promoting effect of dietary polyunsaturated fat on pancreatic carcinogenesis via an accelerated prostaglandin synthesis, caused by metabolism of LA-derived arachidonic acid in (pre)neoplastic tissue. The purpose of the present study was to investigate whether dietary LA is the cause of pancreatic tumor promotion by a high fat diet. Five groups of 30 azaserine-treated rats and 5 groups of 30 N-nitrosobis(2-oxopropyl)amine-treated hamsters were maintained for 6 months (rats) and 12 months (hamsters) on high fat (25 weight %) AIN diets containing 2, 4, 6, 10, or 15 weight % LA. The results indicated that the strongest enhancing effect on the growth of pancreatic (pre)neoplastic lesions in rats and hamsters was obtained with 4 and 2 weight % of dietary LA, respectively. At higher LA levels the tumor response seemed to decrease rather than increase. In both rats and hamsters the fatty acid profiles of blood plasma and pancreas showed an accurate reflection of the dietary fatty acid profiles: a proportional increase in LA levels was observed in plasma and pancreas with increasing dietary LA. In both species plasma and pancreatic AA levels remained constant, except for arachidonic acid levels in rat plasma, which significantly increased with increasing dietary LA levels. Fatty acid profiles in hamster pancreatic tumors did not differ from fatty acid profiles in nontumorous pancreatic tissue from hamsters fed the same diet. Prostaglandin (PG) E2, 6-keto-PGF1 alpha, PGF2 alpha, and thromboxane B2-concentrations in nontumorous pancreatic tissue were similar among the diet groups. Ductular adenocarcinomas from hamster pancreas showed significantly higher levels of 6-keto-PGF1 alpha, PGF2 alpha, and thromboxane B2, but not of PGE2 in comparison with nontumorous pancreas. It is concluded that the strongest pancreatic tumor promotion by dietary LA is 4 weight % in rats and 2 weight % or less in hamsters, and that PGs may be involved in the development of ductular adenocarcinomas induced in hamster pancreas by N-nitrosobis(2-oxopropyl)amine.

Animals↗
PubMed1994

Conjugated linoleic acid. A powerful anticarcinogen from animal fat sources.

Conjugated linoleic acid (CLA) is a mixture of positional and geometric isomers of linoleic acid, which is found preferentially in dairy products and meat. Preliminary studies indicate that CLA is a powerful anticarcinogen in the rat mammary tumor model with an effective range of 0.1-1% in the diet. This protective effect of CLA is noted even when exposure is limited to the time of weaning to carcinogen administration. The timing of this treatment corresponds to maturation of the mammary gland to the adult stage, suggesting that CLA may have a direct effect in reducing the cancer risk of the target organ. Of the vast number of naturally occurring substances that have been demonstrated to have anticarcinogenic activity in experimental models, all but a handful of them are of plant origin. Conjugated linoleic acid is unique because it is present in food from animal sources, and its anticancer efficacy is expressed at concentrations close to human consumption levels.

Animals↗
PubMed1986

Effects of linoleic acid and gamma-linolenic acid intake on platelet functions in elderly people.

Sixteen old subjects were given daily dietary supplement of lg of linoleic acid and lg of gamma-linolenic acid (primerose oil) or 2g of linoleic acid (sunflower oil) for periods of two months. Haemostatic parameters, platelet aggregation, exogenous and endogenous arachidonic acid metabolism were investigated before and after the intake. Diets did not induce any significant change in haemostatic parameters (bleeding time, levels of anti-thrombin III, plasminogen and plasma beta-TG and PF4). Platelet rich plasma aggregation induced by collagen and arachidonic acid were significantly reduced after linoleic acid (18:2n-6) intake. In contrast, gamma-linolenic acid (18:3n-6) supplement did not alter aggregation. However, thromboxane B2 formation (under stimulation) and vitamin E level in platelets (but not in plasma) were decreased after 18:3n-6 as compared to 18:2n-6 intake. The mechanism of thromboxane B2 decrease is unclear. Nevertheless, we may speculate that beneficial effect of this decrease could be counterbalanced by the decreased platelet vitamin E. We conclude that intake of 18:2n-6 or 18:3n-6 does not affect much platelet functions in elderly people.

8,11,14-Eicosatrienoic Acid↗
PubMed1998

Linoleic acid and alpha-linolenic acid lightens ultraviolet-induced hyperpigmentation of the skin.

This study was conducted to evaluate the effects of unsaturated fatty acids on ultraviolet-induced hyperpigmentation of the skin. An efficient lightening effect was observed following topical application of linoleic acid or alpha-linolenic acid to UV-stimulated hyperpigmented dorsal skin of brownish guinea pigs. The number of melanocytes in the treated skin was similar to the number in the skin of the pigmented control, indicating that the pigment-lightening effect was not due to depletion of melanocytes. In vitro experiments using cultured murine melanoma cells showed that melanin production was inhibited most effectively by alpha-linolenic acid, followed by linoleic acid and then by oleic acid. Furthermore, the turnover of the stratum corneum, which plays an important role in the removal of melanin pigment from the epidermis, was accelerated by linoleic acid and by alpha-linolenic acid. Taken together, the results suggest that the pigment-lightening effects of linoleic acid and alpha-linolenic acid are, at least in part, due to suppression of melanin production by active melanocytes, and to enhanced desquamation of melanin pigment from the epidermis.

Administration, Topical↗
PubMed2004

Formation of volatile compounds in model experiments with crude leek (Allium ampeloprasum Var. Lancelot) enzyme extract and linoleic acid or linolenic acid.

Three continuous assays are described for lipoxygenase (LOX), hydroperoxide lyase (HPL) and alcohol dehydrogenase (ADH) in leek tissue. The catalytic activity of LOX showed significant difference (significance level 5%) between linolenic acid (9.43 x 10(-)(4) katals per kg protein) and linoleic acid (2.53 x 10(-)(4) katals per kg protein), and the pH-optimum of LOX was 4.5-5.5 against linoleic acid. The catalytic activity of HPL was statistically the same for 9-(S)-hydroperoxy-(10E,12Z)-octadecadienoic acid (1.01 x 10(-)(2) katals per kg protein) and 13-(S)-hydroperoxy-(9Z,11E)-octadecadienoic acid (7.69 x 10(-)(3) katals per kg protein). ADH showed a catalytic activity of 5.01 x 10(-)(4) katals/kg of protein toward hexanal. Model experiments with crude enzyme extract from leek mixed with linoleic acid or linolenic acid demonstrated differences in the amount of produced aroma compounds. Linoleic acid resulted in significantly most hexanal, heptanal, (E)-2-heptenal, (E)-2-octenal, (E,E)-2,4-decadienal, pentanol, and hexanol, whereas linolenic acid resulted in significantly most (E)-2-pentenal, (E)-2-hexenal, (E,Z)-2,4-heptadienal, (E,E)-2,4-heptadienal, and butanol. Leek LOX produced only the 13-hydroperoxide of linoleic acid and linolenic acid.

Alcohol Dehydrogenase↗
PubMed2004

Effects of conjugated linoleic acid isomers on lipid metabolism and gluconeogenesis in monolayer cultures of bovine hepatocytes.

The objective was to determine the effects of linoleic acid and different isomers of conjugated linoleic acid (CLA) at different concentrations on hepatic lipid and glucose metabolism in the bovine. Monolayer cultures of hepatocytes obtained from 7- to 10-d-old Holstein bull calves were exposed to treatments from 16 to 64 h after plating. The treatments included 1.0 mM palmitic acid plus either 0.1 or 1.0 mM of cis-9, cis-12 linoleic acid, cis-9, trans-11 CLA, or trans-10, cis-12 CLA. Metabolism of palmitic acid to cellular triacylglycerol (TAG) was decreased when media contained cis-9, trans-11 compared with trans-10, cis-12 CLA. Total cellular TAG content was increased for the CLA isomers compared to cis-9, cis-12 linoleic acid. Both CLA isomers increased palmitic acid incorporation into phospholipids, cholesterol, and media triacylglycerol compared with cis-9, cis-12 linoleic acid at a concentration of 1.0 mM. Increasing the concentration of treatment fatty acids from 0.1 to 1.0 mM decreased oxidation of palmitic acid to acid-soluble products, but no effects of fatty acids were observed. There was no treatment effect on rates of gluconeogenesis from propionic acid. Overall, CLA isomers elicited changes in palmitic acid metabolism to cellular and media triacylglycerol, and cellular phospholipids and cholesterol, but had little or no effect on other measured pathways of lipid metabolism or gluconeogenesis in bovine hepatocytes.

Animals↗