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PubMed1991

Linoleic acid chyloportal partition and metabolism during its intestinal absorption.

1-14C linoleic acid intestinal absorption and simultaneous biochemical events were followed up on rats under vascular perfusion and on main mesenteric lymphatic duct fistulated rats. 1-14C linoleic acid was introduced in the duodenum alone in doses from 1.2 to 90 mumol or in the presence of oleic acid and monopalmitin (30/30/30 mumol/mumol/mumol). Mesenteric portal venous blood and chyle, respectively, were collected continuously for 1 and 6 h after the infusions. Blood-labeled lipid recovery varied from 4.7 to 2.2% of the 14C linoleic acid infused as the 14C linoleic acid dose infused increased, and dropped to 1.8% with the mixed lipid infusate. Lymph-labeled lipid recovery increased from 25.7 to 31.8% of the 14C linoleic acid infused as the dose infused increased, and rose to 48.1% with the mixed lipid infusate. The oxidation of 1-14C linoleic acid remained low: 0.8-3% of the infused radioactivity. A desaturation and elongation of 14C linoleic acid into 14C arachidonic acid was detected and discussed. We can conclude that the linoleic lymph absorption pathway remained preferential in our experimental conditions, simultaneous to a low rate of oxidation and an eventual ability for the enterocyte to convert this essential fatty acid arachidonic acid.

Animals↗
PubMed2006

The regulation of formation of prostaglandins and arachidonoyl-CoA from arachidonic acid in rabbit kidney medulla microsomes by linoleic acid hydroperoxide.

Under physiological conditions, small amounts of free arachidonic acid (AA) are released from membrane phospholipids, and cyclooxygenase (COX) and acyl-CoA synthetase (ACS) competitively act on this fatty acid to form prostaglandins (PGs) and arachidonoyl-CoA (AA-CoA). In the present study, we investigated the effects of linoleic acid (LA) and 13-hydroperoxyoctadecadienoic acid (13-HPODE) on the PG and AA-CoA formation from high and low concentrations of AA (60 and 5 microM) in rabbit kidney medulla microsomes. The kidney medulla microsomes were incubated with 60 or 5 microM [(14)C]-AA in 0.1M Tris-HCl buffer (pH 8.0) containing cofactors of COX (reduced glutathione and hydroquinone) and cofactors of ACS (ATP, MgCl(2) and CoA). After incubation, PG (as total PGs), AA-CoA and residual AA were separated by selective extraction using petroleum ether and ethyl acetate. LA (10-50 microM) reduced only PG formation from both 60 and 5 microM AA. 13-HPODE (10-50 microM) also reduced PG formation from 60 and 5 microM AA, but the inhibitory potency was much stronger than that by LA. Furthermore, 13-HPODE had the potential to increase the AA-CoA formation with a decrease in the PG formation from 5 microM AA. These results suggest that 13-HPODE, but not LA, may shift AA away from COX pathway into ACS pathway under low substrate concentration (near physiological concentration of AA).

Acyl Coenzyme A↗
PubMed2002

Ricinoleic acid and castor oil as substrates for conjugated linoleic acid production by washed cells of Lactobacillus plantarum.

Ricinoleic acid (12-hydroxy-cis-9-octadecaenoic acid) was an effective substrate for conjugated linoleic acid (CLA) production by washed cells of Lactobacillus plantarum AKU 1009a. The CLA produced was a mixture of cis-9,trans-11- and trans-9,trans-11-octadecadienoic acids. Addition of alpha-linolenic acid to the culture medium increased the CLA productivity of the washed cells. In the presence of lipase, castor oil, in which the main fatty acid component is ricinoleic acid, also was a substrate for CLA.

Castor Oil↗
PubMed1996

Effect of linoleic acid intake on growth of infants with cystic fibrosis.

Essential fatty acid deficiency as a result of inadequate linoleic acid impairs growth in healthy infants and is common in infants with malabsorption due to cystic fibrosis (CF). We investigated the effect of dietary linoleic acid intake on the growth of infants with CF. In this study, predigested formula preparations A and B, with linoleic acid contents of 12% and 7% of energy, respectively, were fed before and after 1989 to infants enrolled in the evaluation and treatment protocol of the Wisconsin CF Neonatal Screening Project. Outcome was assessed from height-for-age (HAZ) and weight-for-age (WAZ) Z scores on follow-up exams during the first year. Baseline characteristics did not differ significantly between groups A (n = 43) and B (n = 33). At diagnosis, 53% of the enrolled infants (n = 76) showed low plasma linoleic acid concentrations and 22% had a high ratio of triene to tetraene. After correcting for the effect of potentially confounding variables, we found that HAZ (by .27, P < 0.05) and WAZ (by 0.26, P = 0.081) were higher in group A than in group B. This occurred despite a significantly higher energy intake in group B. This difference was most pronounced between 6 and 9 mo of age. Our results suggest that a high linoleic acid content in formula benefits infants with CF because it optimizes nutrition, growth, and feeding efficiency.

Age Factors↗
PubMed2004

Long-chain conversion of [13C]linoleic acid and alpha-linolenic acid in response to marked changes in their dietary intake in men.

We studied the long-chain conversion of [U-13C]alpha-linolenic acid (ALA) and linoleic acid (LA) and responses of erythrocyte phospholipid composition to variation in the dietary ratios of 18:3n-3 (ALA) and 18:2n-6 (LA) for 12 weeks in 38 moderately hyperlipidemic men. Diets were enriched with either flaxseed oil (FXO; 17 g/day ALA, n=21) or sunflower oil (SO; 17 g/day LA, n=17). The FXO diet induced increases in phospholipid ALA (>3-fold), 20:5n-3 [eicosapentaenoic acid (EPA), >2-fold], and 22:5n-3 [docosapentaenoic acid (DPA), 50%] but no change in 22:6n-3 [docosahexanoic acid (DHA)], LA, or 20:4n-6 [arachidonic acid (AA)]. The increases in EPA and DPA but not DHA were similar to those in subjects given the SO diet enriched with 3 g of EPA plus DHA from fish oil (n=19). The SO diet induced a small increase in LA but no change in AA. Long-chain conversion of [U-13C]ALA and [U-13C]LA, calculated from peak plasma 13C concentrations after simple modeling for tracer dilution in subsets from the FXO (n=6) and SO (n=5) diets, was similar but low for the two tracers (i.e., AA, 0.2%; EPA, 0.3%; and DPA, 0.02%) and varied directly with precursor concentrations and inversely with concentrations of fatty acids of the alternative series. [13C]DHA formation was very low (<0.01%) with no dietary influences.

Adult↗
PubMedDate not supplied

Characterization of metabolic pathway of linoleic acid 9-hydroperoxide in cytosolic fraction of potato tubers and identification of reaction products.

Potato tubers are shown to contain a unique lipoxygenase pathway to form 9-hydroperoxy-10,12-octadecadienoic acid (9-HPODE) from linoleic acid. Here, we report the metabolic pathway of 9-HPODE in the cytosolic fraction and the characterization of enzymes involved in the conversion of metabolites. The analysis of enzymatic reaction products at pH 5.5 revealed the formation of 9-keto-10,12-octadecadienoic acid, 9-hydroxy-10,12-octadecadienoic acid, 9,10-epoxy-11-hydroxy-12-octadecenoic acid, 9,10,13-trihydroxy-11-octadecenoic acid, and 9,12,13-trihydroxy-10-octadecenoic acid. The cytosolic enzymes were separated by anion-exchange chromatography into two fractions E1 and E2, having molecular masses of 66 and 54 kDa, respectively. The enzyme fraction E1 only produced 9-keto-10,12-octadecadienoic acid, whereas E2 formed other products. The enzyme E1 showed higher reactivity with 13- and 9-hydroperoxide of alpha-linolenic acid than 9-HPODE, but no reaction with hydroxy fatty acids. In contrast, the enzyme E2 showed the highest reactivity with 9-HPODE, followed by hydroperoxides of alpha-linolenic acid and arachidonic acid. We also evaluated the antibacterial activity of hydroxy fatty acids against Erwinia carotovora T-29, a bacterium infecting potato tubers. Growth of the bacteria was suppressed more potently with 9- or 13-hydroxy fatty acids than dihydroxy or trihydroxy fatty acids, suggesting a role for the metabolites in the resistance of bacterial infection.

Chromatography, Gel↗
PubMed1999

Conjugated linoleic acid content of milk from cows fed different diets.

Conjugated linoleic acid in milk was determined from cows fed different diets. In Experiment 1, cows were fed either normal or high oil corn and corn silage. Conjugated linoleic acid was 3.8 and 3.9 mg/g of milk fatty acids in normal and high oil treatments, respectively. In Experiment 2, cows consumed one-third, two-thirds, or their entire feed from a permanent pasture. Alfalfa hay and concentrates supplied the balance of feed for the one-third and two-third pasture treatments. Conjugated linoleic acid was 8.9, 14.3, and 22.1 mg/g of milk fatty acids in the one-third, two-third, and all pasture treatments, respectively. Cows grazing pasture and receiving no supplemental feed had 500% more conjugated linoleic acid in milk fat than cows fed typical dairy diets (Experiment 1). In Experiment 3, cows were fed either a control diet containing 55% alfalfa silage and 45% grain, or similar diets supplemented with 3% fish meal, or 250 g of monensin/cow/per day, or fish meal and monensin together. Conjugated linoleic acid was 5.3, 8.6, 6.8, and 8.9 mg/g of milk fatty acids in the control, fish meal, monensin, and fish meal plus monensin treatments, respectively. In Experiment 4, cows were fed either finely chopped alfalfa hay (Treatment 1), or coarsely chopped alfalfa hay (Treatment 2) in a 50% forage and 50% grain diet, or 66.6% grass hay and 33.4% grain (Treatment 3), or 98.2% grass hay (Treatment 4). Conjugated linoleic acid was 7.3, 8.3, 9.0, and 7.9 mg/g of milk fatty acids in treatments 1 through 4, respectively.

Animals↗
PubMed1980

Cerebrospinal fluid lipids in demyelinating disease. II. Linoleic acid as an index of impaired blood-CSF barrier.

The absolute linoleic acid concentration in CSF was determined and the findings of MS patients (n = 10) and controls (n = 12) were compared. The linoleic acid content of control CSF (1.6 +/- 0.8 nMol/ml) is considerably lower than the corresponding serum value (2.5--4.1 muMol/ml). Although CSF from MS patients contains a significantly higher linoleic acid concentration than controls the close correlation between CSF linoleic acid and CSF albumin is maintained. The high CSF concentration of cholesterol esters rich in linoleic acid, which are abundant in serum but represent only traces in CNS lipids, points towards an impaired BBB function as the cause of CSF linoleic increase. We are able to show that both albumin and linoleic acid are suitable as "serum markers" and also as reference parameters for the overproportional IgG concentration in the CSF of MS patients. On the basis of these results it can be assumed that changes in CSF linoleic acid content are an expression of dysfunction of the blood-CSF barrier in MS and not, as had previously been postulated, the result of altered myelin metabolism.

Adult↗
PubMed1997

The linoleic acid metabolite, (13S)-hydroperoxyoctadecadienoic acid, augments the epidermal growth factor receptor signaling pathway by attenuation of receptor dephosphorylation. Differential response in Syrian hamster embryo tumor suppressor phenotypes.

In Syrian hamster embryo (SHE) fibroblasts, epidermal growth factor receptor (EGFR) tyrosine kinase activity regulates the metabolism of endogenous linoleic acid to (13S)-hydroperoxyoctadecadienoic acid (13S)-HPODE). (13S)-HPODE stimulates EGF-dependent mitogenesis in a SHE cell phenotype, which expresses tumor suppressor genes (supB+), but was not effective in a variant that does not express these suppressor genes (supB-). In the present study, we have investigated the potential effects of this lipid metabolite on the EGFR signaling pathways in these two SHE cell lines. Treatment of quiescent SHE cells with EGF produced a rapid, transient increase in the tyrosine phosphorylation of EGFR. Dependence on EGF concentration for EGFR tyrosine phosphorylation was similar in both SHE cell lines, but a more prolonged phosphorylation was detected in the supB- variant. Incubation of supB+ cells with (13S)-HPODE and EGF increased EGFR autophosphorylation and tyrosine phosphorylation on several signaling proteins with Src homology-2 domains including GTPase-activating protein. The lipid metabolite did not significantly alter EGF-dependent tyrosine phosphorylation in the supB- variant. Tyrosine phosphorylation of mitogen-activated protein (MAP) kinase was also measured. The addition of (13S)-HPODE increased the extent and duration of MAP kinase tyrosine phosphorylation in supB+ cells but not in the supB- variant. MAP kinase activity in supB+ cells, as measured in immunoprecipitates from cells after the addition of EGF, was increased by the presence of (13S)-HPODE. The addition of (13S)-HPODE did not directly alter EGFR kinase activity or the internalization of the EGFR. However, the addition of (13S)-HPODE to supB+ cells extended the tyrosine phosphorylation of the EGFR in response to EGF. The dephosphorylation of the EGFR was measured directly, and a slower rate was observed in the supB- compared with the supB+ cells. Incubation of the supB+ cells with (13S)-HPODE attenuated the dephosphorylation of the EGFR. Thus, (13S)-HPODE stimulates EGF-dependent mitogenesis and up-regulation of EGF-dependent tyrosine phosphorylation by inhibiting the dephosphorylation of the EGFR. This study shows that a metabolite of an essential dietary fatty acid, linoleic acid, can modulate tyrosine phosphorylation and activity of key signal transduction proteins in a growth factor mitogenic pathway.

Animals↗
PubMed2004

An overview of the effect of linoleic and conjugated-linoleic acids on the growth of several human tumor cell lines.

Both n-6 and n-3 polyunsaturated fatty acids are dietary fats important for cell function, being involved in several physiologic and pathologic processes, such as tumorigenesis. Linoleic acid and conjugated linoleic acid, its geometrical and positional stereoisomer, were tested on several human tumor cell lines originating from different tissues and with different degrees of malignancy. This was to provide the widest possible view of the impact of dietary lipids on tumor development. While linoleic acid exerted different effects, ranging from inhibitory to neutral, even promoting growth, conjugated linoleic acid inhibited growth in all lines tested and was particularly effective against the more malignant cells, with the exception of mammary tumor cells, in which behavior was the opposite, the more malignant cell line being less affected. The inhibitory effect of conjugated linoleic acid on growth may be accompanied by different contributions from apoptosis and necrosis. The effects of conjugated linoleic acid on growth or death involved positive or negative variations in PPARs. The important observation is that a big increase of PPARalpha protein occurred in cells undergoing strong induction of apoptosis, whereas PPARbeta/delta protein decreased. Although PPARalpha and PPARbeta/delta seem to be correlated to execution of the apoptotic program, the modulation of PPARgamma appears to depend on the type of tumor cell, increasing as protein content, when inhibition of cell proliferation occurred. In conclusion, CLA may be regarded as a component of the diet that exerts antineoplastic activity and its effect may be antiproliferative or pro-apoptotic.

Antineoplastic Agents↗
PubMed2000

Mechanisms of action of conjugated linoleic acid: evidence and speculation.

Conjugated linoleic acid (CLA) has been shown to inhibit carcinogenesis and atherosclerosis, enhance immunologic function while protecting against the catabolic effects of immune stimulation, affect body composition change (reducing body fat gain while enhancing lean body mass gain), and stimulate the growth of young rats. We discuss possible biochemical mechanisms that underlie these physiological effects. We emphasize the importance of considering the effects, both individually and combined, of the two CLA isomers (cis-9, trans-11 CLA and trans-10, cis-12 CLA) that have been shown to exhibit biological activity and which appear to exert their effects via different biochemical mechanisms.

Animals↗
PubMed1987

[Oxidative degradation of linoleic acid methyl ester in suspensions of inorganic excipients. 1. Auto-oxidation in the presence of silicic acid products and aluminum oxide].

Linoleic acid methyl ester (LME) was selected as a model to study the autoxidation of unsaturated compounds at the surfaces of inorganic excipients. From IR spectra of LME-silica adsorbates it was concluded that the interaction between LME and the silica surface is mainly due to hydrogen bonds, established between the ester carbonyl and the silica silanol groups. The autoxidation was continuously monitored by measuring the oxygen consumption of LME under UV light exposure and isobaric conditions, and, in parallel, by determining the carbonyl and peroxide values of LME. The oxidative degradation of LME is enhanced by porous and colloidal silicas as well as by colloidal aluminium oxide. From the oxygen consumption and the ratio of intermediates (carbonyls, peroxides) formed during the degradation of LME it was concluded that the prooxidative effect of the inorganic excipients can be attributed to an accelerated reaction of the peroxides of LME.

Aluminum↗
PubMed1999

Biliary phospholipid secretion is not required for intestinal absorption and plasma status of linoleic acid in mice.

Biliary phospholipids have been hypothesized to be important for essential fatty acid homeostasis. We tested this hypothesis by investigating the intestinal absorption and the status of linoleic acid in mdr2 Pgp-deficient mice which secrete phospholipid-free bile. In mice homozygous (-/-) for disruption of the mdr2 gene and wild-type (+/+) mice, dietary linoleic acid absorption was determined by 72 h balance techniques. After enteral administration, [(13)C]-linoleic acid absorption was determined by measuring [(13)C]-linoleic acid concentrations in feces and in plasma. The status of linoleic acid was determined in plasma and in liver by calculating the molar percentage of linoleic acid and the triene:tetraene ratio. Although plasma concentration of [(13)C]-linoleic acid at 2 h after enteral administration was significantly lower in (-/-) compared to (+/+) mice (P</=0.05), net intestinal absorption of dietary linoleic acid or of [(13)C]-linoleic acid was similar in (+/+) and (-/-) mice. Molar percentage of linoleic acid and the triene:tetraene ratio were not different in whole plasma or in liver of (-/-) compared to (+/+) mice. Present data indicate that biliary phospholipids are involved in the rate of appearance in plasma of enterally administered linoleic acid, but are not required for net intestinal absorption or plasma status of linoleic acid.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2005

Milk and cheese fatty acid composition in sheep fed Mediterranean forages with reference to conjugated linoleic acid cis-9,trans-11.

Two experiments were undertaken to evaluate the effect on milk and cheese fatty acid composition of feeding different fresh forages to dairy sheep both in winter (experiment 1, growing stage of the forages, early lactating ewes) and in spring (experiment 2, reproduction stage of the forages, midlactating ewes). Four forage species were compared: annual ryegrass (RY, Lolium rigidum Gaudin), sulla (SU, Hedysarum coronarium L.), burr medic (BM, Medicago polymorpha L.), and a daisy forb (CH, Chrysanthemum coronarium L.). The forages were cut twice daily and offered ad libitum to 4 replicate groups of Sarda dairy sheep (groups RY, SU, BM, and CH). The CH forage was particularly rich in linoleic acid in both periods, whereas BM and SU forages were rich in linolenic acid in winter and spring, respectively. Milk fatty acid composition was affected by the forage in both experiments. Milk conjugated linoleic acid and vaccenic acid contents were higher in CH and BM groups (winter) and CH group (spring) than in the other groups. No differences were observed when comparing fatty acid profile between milk, 1-d-old cheeses, and 60-d-old cheeses within experimental groups, suggesting that the fatty acid recovery rates during cheese making and ripening were not affected by the feeding regimens. After stepwise discriminant analyses of the pooled data, the milks and cheeses sourced in the different feeding regimens differed among them. Based on these results, we conclude that it is possible to manipulate the fatty acid profile of sheep dairy produce to maximize the content of beneficial fatty acids by the use of appropriate fresh forage-based regimens.

Animals↗
PubMed1987

Absorption and lymphatic transport of exogenous and endogenous arachidonic and linoleic acid in the rat.

[3H]Arachidonic (20:4) and [14C]linoleic acid (18:2) were fed to thoracic duct-cannulated rats in test meals of either tracers alone, cream, Intralipid, pure arachidonic acid, or pure linoleic acid. Less [3H]20:4 than [14C]18:2 was recovered in chyle during the first 5 h. After cream feeding, the proportion of radioactivity found in phospholipids was high and increased during the first 3 h. After the meal (3-5 h) 61 +/- 6% of the 3H and 57 +/- 10% of the 14C was in phosphatidylcholine, and 11 +/- 3% of the 3H and 3.0 +/- 4% of the 14C was in phosphatidylethanolamine. Changing the fat vehicle to Intralipid or pure 18:2 decreased the proportion of label in the phospholipids and increased the 3H and 14C radioactivity in the triacylglycerol fraction, the distribution of 14C being influenced more than that of 3H. After feeding the tracers in 200 microliters of pure 20:4, greater than 90% of both isotopes was in triacylglycerol. During fasting, triacylglycerol transported 56% (0.7 mumol/h), phosphatidylcholine transported 34% (0.4 mumol/h), and phosphatidylethanolamine transported 10% (0.1 mumol/h) of the 20:4 mass. After cream or Intralipid feeding, the output of 20:4-containing phosphatidylcholine and phosphatidylethanolamine increased 2.1- to 2.8-fold, whereas the transport of 20:4 with triacylglycerol remained constant. Phospholipids thus became the predominant transport form for 20:4. After feeding 200 microliters of 20:4, the intestine produced, however, 20:4-rich triacylglycerols that transported 89% of the chyle 20:4.

Animals↗
PubMed1981

Degradation of linoleic acid hydroperoxides by a cysteine . FeCl3 catalyst as a model for similar biochemical reactions. II. Specificity in formation of fatty acid epoxides.

1. The degradation of linoleic acid hydroperoxide by cysteine and FeCl3 resulted in formation of a number of oxygenated fatty acids, among which isomeric epoxyoxooctadecenoic and epoxyhydroxyoctadecenoic acids were major products. Pure isomeric hydroperoxides, either 13-L(S)-hydroperoxy-cis-9,trans-11-octadecadienoic acid or 9-D(S)-hydroperoxy-trans-10,cis-12-octadecadienoic acid, were transformed into either 12,13-epoxides or 9,10-epoxides, respectively. 2. From 13-L(S)-hydroperoxy-cis-9,trans-11-octadecadienoic acid, the epoxides were identified as trans-12,13-epoxy-9-oxo-trans-10-octadecenoic acid, trans-12,13-epoxy-9-hydroxy-trans-10-octadecenoic acid, cis-12,13-epoxy-9-oxo-trans-10-octadecenoic acid, trans-12,13-epoxy-erythro-11-hydroxy-cis(trans)-9-octadecenoic acid and trans-12,13-epoxy-threo-11-hydroxy-cis(trans)-9-octadecenoic acid. 3. The 12,13-epoxides were found to be optically active, indicating that the chiral center of the 13-L(S)-hydroperoxy carbon was retained. 4. Although many epoxy fatty acids previously have been identified as linoleic acid hydroperoxide products, this study reports a more complete structural analysis of the various epoxides and allows an assessment of the mechanisms of their formation from hydroperoxides.

Catalysis↗
PubMed1995

Reinvestigation of the antioxidant properties of conjugated linoleic acid.

Despite repeated suggestions that antioxidant activity of conjugated linoleic acid (CLA), a collective of conjugated dienoic isomers of linoleic acid, underlies its reported anticarcinogenic and antiatherosclerotic effects, the antioxidant properties of CLA remain ill-defined. Therefore, this study was undertaken to gain more insight into the mechanism of potential CLA antioxidant activity. It was tested whether CLA could protect membranes composed of 1-palmitoyl-2-linoleoyl phosphatidylcholine (PLPC) from oxidative modification under conditions of metal ion-dependent or -independent oxidative stress. Progress of oxidation was determined by direct spectrophotometric measurement of conjugated diene formation and by gas chromatographic/mass spectrometric analysis of fatty acids. The oxidative susceptibility of CLA was higher than that of linoleic acid, and comparable to arachidonic acid. When oxidation of PLPC (1.0 mM) was initiated using the lipid-soluble 2,2'-azobis(2,4-dimethylvaleronitrile) or the water-soluble 2,2'-azobis(2-amidinopropane) hydrochloride, the radical scavengers vitamin E and butylated hydroxytoluene (BHT) at 0.75 microM efficiently inhibited PLPC oxidation, as evident from a clear lag phase. In contrast, 0.75 microM CLA did not have any significant effect on PLPC oxidation. Inhibition of PLPC oxidation by higher concentrations of CLA appeared due to competition, not to an antioxidant effect. When oxidation of PLPC was initiated by hydrogen peroxide/Fe2+ (500 microM/0.05-20 microM), both vitamin E (1 microM) and ethylene glycol-bis(aminoethyl ether) tetraacetic acid (50 microM) efficiently inhibited PLPC oxidation. However, CLA (1-50 microM) did not show a clear protective effect under any of the conditions tested. We conclude that CLA, under these test conditions, does not act as an efficient radical scavenger in any way comparable to vitamin E or BHT. CLA also does not appear to be converted into a metal chelator under metal-ion dependent oxidative stress, as had previously been suggested. On the basis of our observations, a role for CLA as an antioxidant does not seem plausible.

Antioxidants↗
PubMed2006

Isomer-specific anti-obese and hypolipidemic properties of conjugated linoleic acid in obese OLETF rats.

Conjugated linoleic acid (CLA), a mixture of positional and geometric isomers of linoleic acid, has attracted considerable attention because of its potentially beneficial biologic effects both in vitro and in vivo. Our results clearly show the specific action of the 10trans,12cis-CLA isomer against hyperlipidemia and obesity in obese Otsuka Long-Evans Tokushima Fatty (OLETF) rats. After 2 weeks of feeding with 10t,12c-CLA, but not 9cis,11trans-CLA, abdominal adipose tissue weight and serum and hepatic lipid levels in OLETF rats were lower than those in linoleic acid-fed rats. These effects were attributable to suppressed fatty acid synthesis and enhanced fatty acid beta oxidation in the liver on a 10t,12c-CLA diet. Additionally, we showed that mRNA expression of fatty acid synthase, carnitine palmitoyltransferase, leptin, and sterol regulatory element binding protein-1 was also regulated by 10t,12c-CLA. We suppose that 10t,12c-CLA reveals hypolipidemic and anti-obese activity through the alteration of mRNA expressions in the liver and white adipose tissue.

Adipose Tissue↗