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PubMed2003

Conjugated linoleic acids alter the fatty acid composition and physical properties of egg yolk and albumen.

Effects of dietary conjugated linoleic acids (CLAs) and docosahexaenoic acid (DHA) on the fatty acid composition of different egg compartments after storage were studied. Four dietary treatments [supplemented with safflower oil (SAFF, control group), DHA, CLAs plus DHA (CAD), and CLAs alone] were administered to Single Comb White Leghorn (SCWL) laying hens. Eggs from the different treatment groups were collected and stored for 10 weeks at 4 degrees C before analysis. Fatty acids from the yolk (yolk granules and plasma), egg albumen, and vitelline membrane were analyzed by gas chromatography. The yolk of eggs from hens given CLAs had significantly higher amounts of saturated fatty acids, typically 16:0 and 18:0, but lower amounts of polyunsaturated fatty acids (PUFAs) compared to eggs from the control group (SAFF). CLA content was highest in the yolk and present in both neutral and polar lipids, with the greatest concentrations in neutral lipids. DHA was incorporated mainly into yolk polar lipids. Lipids in yolk plasma and granules contained similar amounts of CLAs. The fatty acid compositions of vitelline membrane and egg albumen mirrored that of the egg yolk. CLA supplementation resulted in hard and rubbery yolks when compared to hard-cooked eggs from the control group. This study showed that feeding CLAs to hens led to accumulation of the isomers in polar and neutral lipids of the egg yolk and that these isomers migrated into egg albumen. Because the sensory properties of hard-cooked eggs were negatively affected by the enrichment of a mixture of CLA isomers in this study, further research should be conducted to evaluate how the different isomers alter the properties of egg yolk and albumen so that the quality of designed eggs containing CLAs and DHA can be improved.

Animals↗
PubMed2000

Effects of conjugated linoleic acid. 1. Fatty acid modification of yolks and neonatal fatty acid metabolism.

The purpose of this study was to evaluate the effects of conjugated linoleic acids (CLA) on neonatal fatty acid metabolism. In this study, layer hens (n = 40) were divided into four equal groups and subjected to the following treatments. Group A served as the control group, Group B received 1 g CLA every other day, Group C received 1 g CLA every 4th d, and Group D was sham-supplemented with 1 g safflower oil every other day. After 4 mo of feeding, Group B hens exhibited an increase in BW and egg size; however, there were no differences noted in feed consumption among the various treatment groups. At the same time, hens were inseminated with a constant dose of pooled rooster semen to evaluate changes in chick liver and yolk fatty acid metabolism during neonatal growth. At hatch and through 6 d of age, there were no significant differences in breakout data (fertility and numbers of early-, mid-, or late-dead chicks) or chick BW, respectively. However, Group B chicks exhibited an increase in liver 18:3n3 and 22:1n9 and a decrease in 20:3n6 and 22:5n3 fatty acids when compared with chicks from Groups A and D. Also noted for Group B chicks, yolk 18:0 fatty acid was higher than that for Group A and D chicks. These results suggest that CLA alters lipid metabolism in growing chicks.

Animals↗
PubMed1996

Assessments on the digestibility of oxidized compounds from [1-14C] linoleic acid using a combination of chromatographic techniques.

The aim of this study was to evaluate the digestibility coefficients of different groups of oxidized fatty acids by applying a methodology based on chromatographic techniques. After thermoxidative treatment, oxidized labelled linoleic acid was isolated and included at 1% in the experimental diets. Male 250-300 g Wistar rats were fed ad lib for seven days. Lipids extracted from diets and faeces were analyzed using a combination of chromatographic methods and radioactivity measurements to determine the specific digestibilities of four groups of altered fatty acids: oxidized monomers non-polar dimers, oxidized dimers and polymers. Mean digestibility coefficients of oxidized monomers, dimers and polymers were 91.0, 74.5 and 69.8%, respectively. In contrast, non-polar dimers were poorly absorbed. The presence of unaltered labelled fatty acids in faeces indicated that structural modifications may have been taken place prior to absorption, and oxidized fatty acids seem to be the main compounds affected.

Animals↗
PubMed1998

Linoleic acid peroxidation by Solanum tuberosum lipoxygenase was activated in the presence of human 5-lipoxygenase-activating protein.

The present investigation describes the ability of human 5-lipoxygenase-activating protein (FLAP) to activate a plant 5-lipoxygenase. The presence of an active recombinant human FLAP in the 100000xg membrane fraction of infected Sf9 cells led to a specific increase in 9-hydroperoxyoctadecadienoic acid (9-HPOD) synthesis (+68%) or in 5-hydroperoxyeicosatetraenoic acid (5-HPETE) synthesis (+68%), after action of Solanum tuberosum tuber 5-lipoxygenase (S.t.LOX) on linoleic acid (natural plant lipoxygenase substrate) or on arachidonic acid. On the contrary, the presence of non-transfected membranes obtained from non-infected Sf9 cells led to an inhibition of lipoxygenase activity. MK-886, a potent inhibitor of leukotriene biosynthesis, blocked the FLAP dependent S.t.LOX activation after preincubation with FLAP transfected membranes. In conclusion, this study demonstrates that a recombinant human FLAP can stimulate a lipoxygenase other than mammalian 5-lipoxygenase (S.t.LOX) by using different polyunsaturated fatty acids as substrates.

5-Lipoxygenase-Activating Proteins↗
PubMed2002

Dietary supplementation with conjugated linoleic acid does not improve nutritional status of tumor-bearing rats.

Tumor necrosis factor-alpha (TNF) is an immunoregulatory cytokine that plays a major role in tumor-induced anorexia and weight loss. Conjugated linoleic acids (CLA) are naturally occurring isomers of linoleic acid that, when added to the diet, improve food intake and body weight in mice injected with TNF. The purpose of the present study was to examine the effects of a diet supplemented with 0.5% CLA on the nutritional status of rats implanted with the Morris 7777 hepatoma. Body weight, food intake, serum levels of insulin-like growth factor, and splenocyte synthesis of TNF were not different in tumor-bearing animals fed CLA versus the control diet. However, insulin levels were increased in both tumor-bearing and control animals given CLA. The 0.5% CLA did not improve the nutritional status nor alter TNF synthesis in hypophagic tumor-bearing rats. The biological significance of increased insulin levels in animals given CLA remains to be determined.

Analysis of Variance↗
PubMed2001

Peroxidation of linoleic acid and its relation to aging and age dependent diseases.

Cell proliferation, cell injury and aging are connected with changes in the cell membrane structure. Apparently these changes activate, in mammalian as well as in plant cells, lipases which liberate polyunsaturated fatty acids (PUFAs). PUFAs are the substrates for lipoxygenases which convert them to corresponding hydroperoxides (LOOHs). Lipoxygenases commit suicide by releasing iron ions. LOOHs react with iron ions to generate radicals. Thus, a nonenzymic lipid peroxidation process (LPO) is induced. It is speculated that the change from enzymic to nonenzymic LPO is connected with the switch from apoptosis to necrosis and that LOOHs produced in enzymic reactions are degraded specifically to signal compounds which induce physiological responses, while nonenzymic reactions seem to induce generation of reactive oxygen species, cell death and age related diseases. Enzymic and nonenzymic LPO processes concern all PUFAs not only arachidonic acid. The main PUFA in mammals is linoleic acid. Since these products serve signalling functions, different degradation paths of linoleic-hydroperoxides are described in detail and the physiological properties of LPO products are discussed in relation to aging and age related diseases.

Aging↗
PubMed1995

Action of linoleic acid on phospholipase C activity at the rectal level of the African locust under the control of protein kinase C.

Linoleic acid (18:2n-6), linolenic acid and eicosatrienoic acid stimulated fluid reabsorption in locust rectum. Only 18:2n-6 was able to enhance phospholipase C activity, inositol(1,4,5) trisphosphate production and to increase cytosolic free Ca2+ concentrations in epithelial cells via the opening of L-type Ca2+ channels. These effects resemble those exerted by neuroparsin, an antidiuretic neuronal hormone extracted from the storage lobes of the locust corpora cardiaca. As for neuroparsin, the effects of 18:2n-6 were abolished after pre-treatment with the protein kinase C inhibitor, polymyxin B. The results were consistent with a regulation of neuroparsin-sensitive phospholipase C activity by 18:2n-6 under control of protein kinase C, possibly by increasing membrane fluidity. Cyclooxygenase inhibitors attenuated the effects of 18:2n-6. This demonstrated that the results should be produced via the metabolites of 18:2n-6 HODEs rather than the PUFA itself.

8,11,14-Eicosatrienoic Acid↗
PubMed2000

Zinc protects against apoptosis of endothelial cells induced by linoleic acid and tumor necrosis factor alpha.

BACKGROUND: Zinc requirements of the vascular endothelium may be increased in inflammatory conditions, ie, atherosclerosis, in which apoptotic cell death is prevalent. OBJECTIVE: We hypothesized that zinc deficiency may potentiate disruption of endothelial cell integrity mediated by fatty acids and inflammatory cytokines by enhancing pathways that lead to apoptosis and up-regulation of caspase genes. DESIGN: Endothelial cells were maintained in low-serum medium or grown in culture media containing selected chelators, ie, diethylenetriaminepentaacetate or N,N,N', N'-tetrakis(2-pyridylmethyl)-ethylenediamine (TPEN), with or without zinc supplementation. Subsequently, cells were treated with linoleic acid, tumor necrosis factor alpha (TNF-alpha), or both. We studied the effect of zinc deficiency and supplementation on the induction of apoptosis by measuring caspase-3 activity, cell binding of annexin V, and DNA fragmentation. RESULTS: Our results indicated that linoleic acid and TNF-alpha independently, but more markedly in concert, up-regulated caspase-3 activity and induced annexin V binding and DNA fragmentation. Zinc deficiency, especially when induced by TPEN, dramatically increased apoptotic cell death induced by cytokines and lipids compared with control cultures. Supplementation of low-serum- or chelator-treated endothelial cells with physiologic amounts of zinc caused a marked attenuation of apoptosis induced by linoleic acid and TNF-alpha. Morphologic changes of cells observed during zinc deficiency were prevented by zinc supplementation. Media supplementation with other divalent cations (eg, calcium and magnesium) did not mimic the protective role of zinc against apoptosis. CONCLUSIONS: Our data indicate that zinc is vital to vascular endothelial cell integrity, possibly by regulating signaling events to inhibit apoptotic cell death.

Animals↗
PubMed1995

Effects of indomethacin with or without linoleic acid on human breast cancer cells in vitro.

The effect of indomethacin (INDO) with or without the addition of linoleic acid (LA) was investigated in a cultured MDA-MB-231 human breast cancer cell line. It was found that INDO without LA suppressed cell growth and thymidine incorporation; however, with the addition of LA, INDO at low concentration promoted these factors, whereas INDO at higher concentrations suppressed them. On the other hand, INDO with or without the addition of LA reduced the secretion of prostaglandin E (PGE). However, INDO at a low concentration (1 microgram/ml) with the addition of LA increased the secretion of leukotriene B (LTB), while INDO without LA had no effect on the secretion of LTB. When the relationship between cell growth and PGE or LTB concentration was investigated, cell growth was associated with the PGE and LTB concentrations when the cells were treated with INDO and LA, whereas it was associated only with the PGE and LTB concentrations when the cells were treated with INDO and LA, whereas it was associated with the PGE concentration when they were treated with INDO alone.

Breast Neoplasms↗
PubMed1997

Retention of conjugated linoleic acid in the mammary gland is associated with tumor inhibition during the post-initiation phase of carcinogenesis.

Conjugated linoleic acid (CLA) has been reported to have significant activity in inhibiting mammary carcinogenesis. A major objective of this study was to evaluate how changes in the concentration of CLA in mammary tissue as a function of CLA exposure/withdrawal were correlated with the rate of occurrence of mammary carcinomas. Rats treated with a single dose of dimethylbenz[a]anthracene (DMBA) at 50 days of age were given 1% CLA in the diet for either 4 weeks, 8 weeks or continuously following carcinogen administration. No cancer protection was evident in the 4 or 8 week-CLA treatment groups. Significant tumor inhibition was observed only in rats that were given CLA for the entire duration of the experiment (20 weeks). Analysis of CLA in the mammary gland showed that the incorporation of CLA was much higher in neutral lipids than in phospholipids. When CLA was removed from the diet, neutral lipid- and phospholipid-CLA returned to basal values in about 4 and 8 weeks, respectively. The rate of disappearance of neutral lipid-CLA (rather than phospholipid-CLA) subsequent to CLA withdrawal paralleled more closely the rate of occurrence of new tumors in the target tissue. It appears that neutral lipid-CLA may be a more sensitive marker of tumor protection than phospholipid-CLA. However, the physiological relevance of CLA accumulation in mammary lipids is unclear and remains to be determined. A secondary goal of this study was to investigate whether CLA might selectively inhibit clonal expansion of DMBA-initiated mammary epithelial cells with wild-type versus codon 61 mutated Ha-ras genes. Approximately 16% of carcinomas in the control group (without CLA) were found to express codon 61 ras mutation. Although continuous treatment with CLA reduced the total number of carcinomas by 70%, it did not alter the proportion of ras mutant versus wild-type carcinomas, suggesting that CLA inhibits mammary carcinogenesis irrespective of the presence or absence of the ras mutation.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed2004

Effects of conjugated linoleic acid levels and feeding intervals on performance, carcass traits and fatty acid composition of finishing barrows.

Two experiments were conducted to investigate the effects of dietary conjugated linoleic acid (CLA) on performance, carcass traits, fatty acid composition and subcutaneous adipose tissue cellularity in finishing barrows. In Experiment 1, 54 crossbred barrows were allotted to one of three treatments, with six pens per treatment and three barrows in each pen. The pigs were fed a diet containing 0, 2, or 4% CLA oil for 6 weeks. Daily gain (P < 0.01) and feed efficiency (P < 0.01) improved with dietary CLA. Loin muscle area (P = 0.01) and intramuscular fat (P = 0.01) increased while 10th rib fat (P = 0.03) and last rib fat (P = 0.02) thickness decreased with increasing dietary CLA. Total CLA isomers increased (P < 0.01) with increasing dietary CLA. Myristic, palmitic and stearic acid levels were increased while oleic, linoleic, linolenic and arachidonic acid decreased in loin muscle and subcutaneous adipose tissue. In Experiment 2, barrows (n = 54) were allotted to one of two treatments with nine pens per treatment and three pigs in each pen. Pigs were fed a diet supplemented with 4% CLA for 3 or 6 weeks before slaughter. Over the entire experimental period, daily gain and feed efficiency were higher (P < 0.01) when CLA was fed for a longer period. Loin muscle area (P < 0.01) and intramuscular fat (P < 0.01) increased while backfat thickness at the 10th (P = 0.03) and last rib (P = 0.04) decreased when CLA was fed for 6 vs. 3 weeks. The number of cells in subcutaneous adipose tissue was not affected while adipocyte volume decreased (P = 0.01) with longer feeding time on dietary CLA. The increased CLA content of pork from CLA fed pigs provides the pork industry with an opportunity to provide value-added, healthful meat products for human consumption with respect to CLA intake and potential improvements in human health.

Adipose Tissue↗
PubMed1982

Inverse relationship between linoleic acid in serum and in adipose tissue of patients with essential hypertension.

In patients with labile essential hypertension without and with overweight as well as in normotensive controls the fatty acid pattern of serum triglycerides and subcutaneous adipose tissue was estimated by gas liquid chromatography. In serum triglycerides of hypertensives linoleic acid was increased but appeared decreased in depot fat. This inverse relationship could not be found for arachidonic acid. Correspondingly, the C 18:2/C 20:4-ratio was higher in serum triglycerides than in adipose tissue. Only in depot fat of overweight hypertensives the percentage of arachidonic acid was decreased when compared to subjects with normal body weight. Linolenic acid remained unchanged in serum triglycerides but decreased significantly in adipose tissue of hypertensive patients. Eicosapentaenoic acid was increased in serum triglycerides and depot fat of patients with essential hypertension of normal body weight. The results are discussed with respect to the possible pathogenesis of essential hypertension and the hypotensive potency of dietary linoleic acid which has been described in patients with high blood pressure.

Adipose Tissue↗
PubMed1988

Hydroperoxides produced by n-6 lipoxygenation of arachidonic and linoleic acids potentiate synthesis of prostacyclin related compounds.

In a previous paper we reported that arachidonic acid (20:4(n-6] strongly enhances the endothelial cell synthesis of prostaglandin I3 (PGI3) from eicosapentaenoic acid (20:5(n-3], in stimulating the cyclooxygenase rather than the prostacyclin synthase (Bordet et al. (1986) Biochem. Biophys. Res. Commun. 135, 403-410). In the present study, endothelial cell monolayers were co-incubated with exogenous 20:5(n-3) or docosatetraenoic acid (22:4(n-6], and n-6 lipoxygenase products of 20:4(n-6) or linoleic acid (18:2(n-6], namely 15-HPETE and 13-HPOD, respectively. Prostaglandins or dihomoprostaglandins were then measured by gas chromatography-mass spectrometry. Both hydroperoxides, up to 20 microM, stimulated the cyclooxygenation of 20:5(n-3) and 22:4(n-6), in particular the formation of PGI3 and dihomo-PGI2, respectively. Higher concentrations inhibited prostacyclin synthetase. In contrast, the reduced products of hydroperoxides, 15-HETE and 13-HOD, failed to stimulate these cyclooxygenations, 13-HPOD appeared more potent than 15-HPETE and the cyclooxygenation of 22:4(n-6) seemed to require higher amounts of hydroperoxides to be efficiently metabolized than 20:5(n-3). These data suggest that prostacyclin potential of endothelium might be enhanced by raising the peroxide tone.

Arachidonic Acid↗
PubMed1982

Low dietary intake of linoleic acid predisposes to myocardial infarction.

Thirty-two men who had recently had a myocardial infarction were matched individually for age with controls who had no evidence of heart disease. The patients had a significantly lower proportion of linoleic acid and a higher proportion of palmitic acid in their plasma triglyceride fatty acids. Analysis of the composition of red-cell membrane phosphatidyl choline, which reflects long-term dietary fat intake, showed a significantly lower proportion of linoleic acid in the patients.These differences suggest that the type of dietary fat consumed might be an important factor in the genesis of ischaemic heart disease.

Adult↗
PubMed2005

Determination of the conjugated linoleic acids in cow's milk fat by Fourier transform Raman spectroscopy.

The collective term "conjugated linoleic acid" or "CLA" generally refers to a mixture of conjugated positional and geometric isomers of linoleic (cis-9,cis-12-octodecadienoic) acid. In nature, these isomers are mainly formed in the rumen by biohydrogenation of polyunsaturated fatty acids. This study concerns a first trial of CLA determination in cow's milk fat by Raman spectroscopy. The spectra of pure cis-9-oleic, cis-9,cis-12-linoleic, cis-9,trans-11-linoleic, and trans-10,cis-12-linoleic acids have been examined in comparison with the spectra of selected milk-fat samples containing between 0 and 3% of CLA. The trial of CLA determination by Raman spectroscopy on cow milk fat has reached its objective with the two following results. First, the examination of the Raman spectra allows to identify three specific Raman signals of the chemical bonds associated to the cis,trans conjugated C=C in the rumenic and trans-10,cis-12-octodecadienoic acids at 1652, 1438, and 3006 cm(-1). Second, the calibration of Raman spectrometer for the CLA determination has indicated that these three specific signals suit very well for the accurate and reliable measurement of CLA concentration in milk fat. To our knowledge, the present study is the first successful attempt to determine the CLA content of milk fat by a spectrophotometric method.

Animals↗
PubMed1982

Oral lecithin and linoleic acid in Friedreich's ataxia: III. Biochemical results.

Lecithin and safflower oil brought about the same changes in serum LAD activity and kinetics in patients with Friedreich's Ataxia as in controls when results of this double-blind crossover study were analyzed according to group assignation. According to functional stages, pretrial LAD activity decreased with advancing severity while Km for lipoamide increased. Lecithin and safflower oil supplements corrected the elevated Km for lipoamide but produced a further reduction in LAD activity. These changes may have been due to the increased intake of linoleic acid, a precursor of lipoic acid, which is present in high percentage in both lecithin and safflower oil. Results of the biochemical study thus agreed with the clinical data gathered during the course of the one-year trial in suggesting that linoleic acid may well have been the active factor through which biochemical and clinical improvement was previously observed in patients with Friedreich's Ataxia supplemented with lecithin.

Administration, Oral↗
PubMed1990

Effect of linoleic acid hydroperoxide on adenovirus DNA replication.

The effect of linoleic acid hydroperoxide on replication of adenovirus type 2 DNA in HeLa cells was examined. The level of the DNA was extremely reduced when the cells immediately after the infection with adenovirus type 2 were incubated for 24 h in the presence of 1 nmol/ml (measured by the thiobarbituric acid reaction and expressed in terms of malondialdehyde) of the hydroperoxide. The levels of the messenger RNA for adenovirus type 2 DNA polymerase and the expressed polymerase were equally reduced. The inhibition of DNA replication by lipid hydroperoxides in animal cells was discussed in relation to degenerative disorders.

Adenoviruses, Human↗
PubMed2005

PPARgamma-dependent effects of conjugated linoleic acid on the human glioblastoma cell line (ADF).

Conjugated linoleic acid (CLA) has been shown to exert beneficial effects against carcinogenesis, atherosclerosis and diabetes. It has been demonstrated that CLA modulates lipid metabolism through the activation of peroxisome proliferator-activated receptors (PPARs). The PPAR family comprises 3 closely related gene products, PPAR alpha, beta/delta and gamma, differing for tissue distribution, developmental expression and ligand specificity. It has also been demonstrated that activated PPARgamma results in growth inhibition and differentiation of transformed cells. These observations stimulated a great interest toward PPARgamma ligands as potential anticancer drugs to be used in a differentiation therapy. Glioblastomas are the most commonly diagnosed primary tumors of the brain in humans. The prognosis of patients with high-grade gliomas is poor and only marginally improved by chemotherapy. The aim of this work was to study the effects of CLA and of a specific synthetic PPARgamma ligand on cell growth, differentiation and death of a human glioblastoma cell line as well as on parameters responsible for the metastatic behavior of this tumor. We demonstrate here that CLA and PPARgamma agonist strongly inhibit cell growth and proliferation rate and induce apoptosis. Moreover, both treatments decrease cell migration and invasiveness. The results obtained show that CLA acts, directly or indirectly, as a PPARgamma activator, strongly suggesting that this naturally occurring fatty acid may be used as brain antitumor drug and as a chemopreventive agent. Moreover, the gamma-agonist, once experimented and validated on man, may represent a useful coadjuvant in glioblastoma therapy and in the prevention of recurrences.

Antineoplastic Agents↗