FATTY ACID COMPOSITION OF THE SERUM LIPIDS OF PIGS GIVEN DIFFERENT AMOUNTS OF LINOLEIC ACID.
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Formation of 9-hydroxy linoleic acid as a product of phospholipid peroxidation in diabetic erythrocyte membranes.
The increased production of oxygen-derived free radicals (OFR) and lipid peroxidation may contribute to vascular complications in diabetes. Some lipid peroxidation products have already been reported to be formed via glucose-induced oxidative stress. We have identified 9-hydroxy linoleic acid (9-OH-C18:2) in the red cell membrane phospholipid of diabetic subjects. We hypothesized that 9-OH-C18:2 would be formed in hydroxyl radical reactions to linoleic acid (C18:2) during glucose-induced oxidative stress, and confirmed that the formation of 9-OH-C18:2 was induced by ultraviolet (UV)-C irradiation to the synthetic C18:2. UV-C light generates highly reactive hydroxy radicals. C18:2 is confirmed to be the precursor of 9-OH-C18:2. To estimate the degree of oxidative damage to red cell membrane phospholipids, we developed a selective ion monitoring gas chromatography-mass spectrometric measurement for C18:2 and 9-OH-C18:2, following methanolysis of red cell membrane phospholipids. The relative peak height ratio of C18:2 to 9-OH-C18:2 (9-OH-C18:2/C18:2) was measured in phospholipid extracts of red cell membranes from healthy (n=29, 3.1+/-1.9%) and diabetic (n=27, 20. 9+/-16.1%) subjects. It was confirmed that 9-OH-C18:2/C18:2 is significantly (P<0.001) elevated in patients with diabetes. The measurement of 9-OH-C18:2/C18:2 in red cell membranes should be useful for assessing oxidative damage to membrane phospholipids in diabetes.
Biomarkers↗
Linoleic acid metabolism in brain cortex of aged rats.
The linoleic acid metabolism was examined in the brain cortex of 4 month-old and 24 month-old rats. After the injection of [1-14C]-linoleate into the lateral ventricle of the brain the animals were sacrificed at 1,3 and 6 hours from the injection. The linoleate (18:2) incorporation into lipids, the presence of fatty acid peroxidation products, as well as the 18:2 transformation into elongated and desaturated derivatives were determined. Both an age-related reduction in linoleate incorporation rate into glycerophospholipids and a decrease in fatty acid turnover were found. Furthermore, in glycerophospholipids from 24 month-old rat brain cortex a higher level of hydroperoxide derivative of linoleate was found as compared to 4 month-old animals, and this damaged fatty acid is eliminated more slowly in aged rats than in adults. Finally, unlike 4 month-old animals, a stimulation of the transformation rate of linoleate into desaturation (6,9,12-C18:3) and elongation (8,11,14,C20:3) products was found in 24 month-old rat brain cortex. On the contrary, as far as arachidonic acid (one of the most important end products of the mechanism of linoleate modification) is concerned, the differences between aged and control animals were small, making it quite difficult to attribute a physiological meaning to this phenomenon.
Aging↗
Effect of dietary conjugated linoleic acid on the growth rate of live birds and on the abdominal fat content and quality of broiler meat.
Two experiments were conducted to investigate the influence of dietary conjugated linoleic acid (CLA) on the growth, body composition, abdominal fat accumulation, and meat quality in broilers. In Experiment 1, 50 broilers that were 3 wk old (total of 200 birds) were assigned to one of the four diets containing 0, 0.25, 0.5, or 1% CLA and were fed for 3 wk. In Experiment 2, 40 broilers that were 3 wk old (total of 120 birds) were assigned to one of the three diets containing 0, 2, or 3% CLA and fed for 5 wk. At the end of the 3-wk feeding trial, the average body weight of broilers for Experiment 1 was about 2.20 kg per bird for all treatments. For Experiment 2, after 5-wk feeding trial, the average body weights of birds were 4.04, 3.99, and 3.93 kg for the control, 2% CLA, and 3% CLA groups, respectively, with a non significant reduction in body weight as the levels of dietary CLA increased. There was no difference in abdominal fat weight, the total body fat, and protein content in broilers among the CLA treatments for Experiment 1. However, when the dietary CLA was increased to 2 or 3%, the total body fat content was reduced. The whole body fat content decreased from 14.2% in the control to 11.9 and 12.2% for 2 and 3% CLA, respectively. Dietary CLA at 2 and 3% levels influenced meat quality. After cooking, the breast meat from 2 or 3% dietary CLA treatment was harder and drier, and the color was a little darker than that of the control. These changes could be caused by the decreased unsaturated fatty acid content in meat after CLA feeding, which increased the melting point of the fat.
Adipose Tissue↗
Effects of trans-10,cis-12 conjugated linoleic acid on body fat and serum lipids in young and adult hamsters.
The aim of the present work was to determine whether t-10, c-12 conjugated linoleic acid (CLA) feeding was able to reduce body fat accumulation and improve the serum lipid profile in adult hamsters fed an atherogenic diet, in order to compare these effects with those observed in young growing hamsters. Young and adult hamsters were fed semi-purified atherogenic diets supplemented with 0.5 % linoleic acid or 0.5% t-10, c-12 CLA for 6 weeks. Body weight and food intake were measured every two days. Adipose tissue from different anatomical locations, liver and gastrocnemious muscle were dissected and weighed. Cholesterol, triacylglycerols, non-esterified fatty acids and proteins were determined spectrophotometrically and water content by gravimetry. In young hamsters, no significant differences were found in food intake, final body weight and gastrocnemious muscle weight. White adipose tissue weights were reduced, liver weight was increased and cholesterol and triacyl-glycerols in both serum and liver were reduced. In adult hamsters, CLA feeding decreased food intake and adipose tissue weights. No changes were observed in other parameters. The present study demonstrates that age has an influence in hamster responsiveness to t-10, c-12 CLA because, although when this isomer is added to an atherogenic diet it reduces body fat accumulation in both young and adults hamsters, the lessening of the effects on serum lipids brought about by atherogenic feeding is only observed in young animals. Moreover, it is clear that liver is a target for CLA in young but not in adult hamsters.
Adipose Tissue↗
Conjugated linoleic acid and hepatic lipogenesis in mouse: role of the mitochondrial citrate carrier.
Conjugated linoleic acid (CLA) is able to reduce adiposity by affecting lipid metabolism. In particular, CLA administration to mice reduces body fat mass with a concomitant lipid accumulation in the liver. We investigated the effects of CLA on the activity of the mitochondrial citrate carrier (CIC), which is implicated in hepatic lipogenesis. The transport activity of the CIC, measured both in intact mitochondria and in the proteoliposomes, progressively increased with the duration of CLA feeding. An increase in the CIC activity of approximately 1.7-fold was found in 16 week CLA-treated mice with respect to control animals. A kinetic analysis showed a 1.6-fold increase in the V(max) of citrate transport but no change in the K(m) value. Western blot experiments revealed an increase of approximately 1.7-fold in the expression of CIC after CLA treatment. A strict correlation between the increase in CIC activity and the stimulation of the cytosolic lipogenic enzymes was also found. These data indicate that the CIC may play a role in the onset of hepatic steatosis in CLA-fed mice by supplying the carbon source for de novo fatty acid synthesis.
Acetyl-CoA Carboxylase↗
Lethal effects of a linoleic acid hydroperoxide and its autoxidation products, unsaturated aliphatic aldehydes, on human diploid fibroblasts.
The lethal effects of linoleic acid and its hydroperoxide on human diploid fibroblasts were quite similar, and that of the reaction mixture from the autoxidation of the hydroperoxide was considerable. Some unsaturated aliphatic aldehydes, the secondary products of the hydroperoxide autoxidation, were identified and their toxicity toward the cells was examined. Among them, (E,E)-2,4-nonadienal, (E,E)-2,4-decadienal, and (E)-4-hydroxy-2-nonenal were the most toxic; e.g., in the presence of 25 microM nonadienal, decadienal, or hydroxynonenal, 75, 90, or almost 100% of the cells, respectively, underwent lysis within one day. Generally, alkenals were toxic and alkanals non-toxic. The toxicity was enhanced as the number of double bonds in each molecule was increased and also as the carbon chain was lengthened.
Aldehydes↗
Trans-10, cis-12- and cis-9, trans-11-conjugated linoleic acid isomers selectively modify HDL-apolipoprotein composition in apolipoprotein E knockout mice.
Trans-10, cis-12-conjugated linoleic acid (CLA)-enriched diets promote atherosclerosis in mice despite increasing blood concentrations of HDL cholesterol. This suggests that under these conditions, the HDL apolipoproteins (apo) produced are abnormal. To test this hypothesis, apoE-deficient mice were fed a Western-type diet enriched with linoleic acid (control), cis-9, trans-11-CLA or trans-10, cis-12-CLA (1.0% wt/wt) for 12 wk, and the effects on HDL metabolism and apoC-III levels recorded. Compared with the control and cis-9, trans-11-CLA mice, those fed the trans-10, cis-12-CLA diet had significantly higher HDL cholesterol concentrations, and had a higher incidence of hypertriglyceridemia and hepatic steatosis. Plasma apoA-I and paraoxonase concentrations were significantly lower in the trans-10, cis-12-CLA group than in the cis-9, trans-11-CLA group. These reductions were associated with decreased hepatic expression of these proteins and a shift toward lipid-poor apolipoprotein particles. The plasma apoA-II concentration increased with its corresponding mRNA concentration in the liver, and was preferentially bound to HDL in the trans-10, cis-12-CLA mice, thus explaining the increased HDL cholesterol concentrations in this group. Significant, positive associations were found between apoA-II and C-III (r=0.883, P<0.001) and between apoA-II and atherosclerosis (r=0.68, P<0.001). These results indicate that trans-10, cis-12-CLA intake modifies HDL to form a proatherogenic apoA-II containing particle and promotes phenotypic changes compatible with metabolic syndrome. Cis-9, trans-11-CLA does not promote this detrimental effect.
Animals↗
Effects of dietary conjugated linoleic acid on lymphocyte function and growth of mammary tumors in mice.
We studied the effects of conjugated linoleic acid (CLA) on lymphocyte function and growth of a transplantable murine mammary tumor. In experiment 1, eight-wk-old female Balb/c mice (n = 8/group) were fed 0.1%, 0.3% or 0.9% CLA for 3 or 6 wk. Lymphocyte proliferation, interleukin-2 production and lymphocyte cytotoxicity were assessed using splenic lymphocytes. Plasma CLA concentrations increased in a dose-dependent manner with CLA feeding. Lymphocyte proliferation in mice fed 0.3% and 0.9% CLA was enhanced in phytohemagglutinin-induced but not in concanavalin A- or lipopolysaccharide-stimulated cultures. Production of IL-2 also was stimulated by CLA. In contrast, CLA had no effect on lymphocyte cytotoxicity. In experiment 2, mice (n = 20/treatment) were fed the same diets for 2 wk before being infused with 1 x 10(6) WAZ-2T metastatic mammary tumor cells into the right inguinal mammary gland. Tumor volume and latency were recorded for 45 d. Dietary CLA did not affect mammary tumor growth. Tumor latency, tumor incidence and tumor lipid peroxidation activity also were unaffected by CLA. Body weight and feed intake were similar among treatments. Therefore, dietary CLA modulated certain aspects of the immune defense but had no obvious effect on the growth of an established, aggressive mammary tumor.
Animals↗
Effects of dietary conjugated linoleic acids on hepatic and muscle lipids in hybrid striped bass.
Conjugated linoleic acids (CLA) are the focus of numerous studies, yet the effects of these isomers of octadecadienoic acids have not been evaluated in many species of fish. In this study, graded amounts of CLA--0, 0.5, 0.75, or 1.0% of the diet--were fed to juvenile hybrid striped bass for 8 wk. Dietary treatments were fed to apparent satiation twice daily to triplicate groups of fish initially weighing 13.4 g/fish. Feed intake and weight gain of fish fed 1.0% CLA were significantly reduced compared to fish fed no CLA. Fish fed 0.5 and 0.75% CLA exhibited reduced feed intake similar to fish fed 1.0% CLA, but had growth rates that were not significantly different from those of fish fed no CLA. Feed efficiency improved significantly in fish as dietary CLA concentrations increased. Total liver lipid concentrations were significantly reduced in fish fed the diets containing CLA compared to those of fish fed the control diet, and intraperitoneal fat ratio was significantly lower in fish fed 1.0% CLA compared to fish fed no CLA. Fish fed dietary CLA exhibited significant increases in hepatosomatic index and moisture content of muscle and carcass. The CLA isomers were detected in liver and muscle of fish fed the diets containing CLA, while a low concentration of one isomer was detected in liver and muscle of fish fed the control diet. Dietary CLA resulted in a significant increase in 18:2(c-9,c-12) concentration in liver and muscle, but a significant reduction in 18:1n-7 in these tissues. Furthermore, feeding CLA resulted in a significant increase in the concentration of 20:5n-3 and 22:6n-3 in liver, but a reduction of these fatty acids in muscle. This study showed that feeding CLA elevated tissue concentrations of these fatty acid isomers, reduced tissue lipid contents, improved feed efficiency, and altered fatty acid concentrations in liver and muscle of fish.
Animal Nutritional Physiological Phenomena↗
Differential incorporation of conjugated linoleic acid isomers into egg yolk lipids.
The incorporation pattern of conjugated linoleic acids (CLA) isomers into the egg yolk of hens in relation to that in the diet was studied. Silver-ion high-performance liquid chromatography (Ag-HPLC) was used to separate individual CLA isomers. It was found that the isomeric distribution pattern in the egg yolk lipids was different from that in the dietary fat. Total cis/trans isomers accounted for 81.2% of total CLA incorporated into the egg yolk, which was in contrast to the value of 92.0% of total CLA in the diet. Total cis/cis isomers accounted for 3.8% total CLA in the diet but they were 6.6% of the total CLA in the egg yolk lipids. In contrast, total trans/trans isomers were 12.2% of the total CLA isomers in the egg yolk lipids, whereas they were only 4.2% of total CLA in the diet. The results showed that total trans/trans-CLA was preferentially incorporated into the egg yolk, whereas the incorporation of total cis/trans-CLA isomers was partially discriminated. Within each group, the incorporation of individual isomers into the egg yolk lipids was also selective. cis-9,trans-11/trans-9,cis-11 and cis-10,trans-12/trans-10,cis-12 were the two major isomers in the diet. Ag-HPLC analysis showed that the former was preferentially transferred into the egg yolk compared with the latter. It was observed that supplementation of CLA in the diet of laying hens decreased the concentration of oleic acid (18:1n-9), arachidonic acid (20:4n-6), and docosahexaenoic acid (22:6n-3) but increased that of linolenic acid (18:3n-3), stearic acid (18:0), and palmitic acid (16:0) in the egg yolk, suggesting that CLA may inhibit Delta6 and Delta9 desaturases.
Animals↗
Conjugated linoleic acids alter milk fatty acid composition and inhibit milk fat secretion in dairy cows.
Conjugated linoleic acids (CLA) have positive health effects in experimental models. Our objective was to determine the effect of CLA supplementation on milk of dairy cows. A commercial source of CLA was infused abomasally to by-pass rumen fermentation. The supplement contained 61.2% CLA; the major CLA isomers were cis/trans 8,10, cis/trans 9,11, cis/trans 10,12 and cis/trans 11,13. Four Holstein cows were used in a 4 x 4 Latin square design. Treatments were 5-d infusions of 0, 50, 100 and 150 g/d of CLA supplement. Infusion increased milk fat content of CLA from 6.8 mg/g fat (zero dose) to 63.6 mg/g fat (highest dose). All of the major CLA isomers in the supplement were transferred to milk fat in a dose-dependent manner. Apparent efficiency of transfer to milk fat was 22.5, 22.5, 10.2 and 26.3% for cis/trans 8,10, cis/trans 9,11, cis/trans 10,12 and cis/trans 11,13, respectively. CLA infusion had no effect on milk protein and little effect on milk yield (21.5, 20.4, 20.9 and 18.3 kg/d for 0, 50, 100 and 150 g/d CLA supplement, respectively). However, CLA infusion dramatically reduced milk fat. On average, the content and yield of milk fat were reduced by 52 and 55%, respectively. The role of specific CLA isomers and mechanism(s) for the reduction in milk fat have not been established, although the pattern of milk fatty acids demonstrated effects were most pronounced on de novo fatty acid synthesis and the desaturation process. Overall, dietary supplemention of CLA increased milk fat content of CLA, altered milk fatty acid composition and markedly reduced the content and yield of milk fat.
Animals↗
Antioxidative effects of flavonols and their glycosides against the free-radical-induced peroxidation of linoleic acid in solution and in micelles.
The antioxidative effect of flavonols and their glycosides against the peroxidation of linoleic acid has been studied in homogeneous solution (tBuOH/H(2)O, 3:2) and in sodium dodecyl sulfate and cetyl trimethylammonium bromide micelles. The peroxidation was initiated thermally by the water-soluble initiator 2,2'-azobis(2-methylpropionamidine) dihydrochloride, and the reaction kinetics were studied by monitoring the formation of linoleic acid hydroperoxides. The synergistic antioxidant effect of the flavonols with alpha-tocopherol (vitamin E) was also studied by following the decay kinetics of alpha-tocopherol and the alpha-tocopheroxyl radical. Kinetic analysis of the antioxidative process demonstrates that the flavonols are effective antioxidants in solution and in micelles, either alone or in combination with alpha-tocopherol. The antioxidative action involves trapping the initiating radicals in solution or in the bulk-water phase of the micelles, trapping the propagating lipid peroxyl radicals on the surface of the micelles, and regenerating alpha-tocopherol by reducing the alpha-tocopheroxyl radical. It was found that the antioxidant activity of the flavonols and their glycosides depends significantly on the position and number of the hydroxy groups, the oxidation potential of the molecule, and the reaction medium. The flavonols bearing ortho-dihydroxy groups possess significantly higher antioxidative activity than those without such functionalities, and the glycosides are less active than their parent aglycones. The activity of the flavonols is higher in micelles than in solution, while the activity of alpha-tocopherol is lower in micelles than in solution. This is because the predominant factor for controlling the activity is the hydrogen-bonding interaction of the antioxidant with the micellar surface in the case of hydrophilic flavonols, while it is the inter- and intramicellar diffusion in the case of lipophilic alpha-tocopherol.
Antioxidants↗
10t,12c-conjugated linoleic acid inhibits lipopolysaccharide-induced cyclooxygenase expression in vitro and in vivo.
Previous data demonstrated that conjugated linoleic acid (CLA) reduced eicosanoid release from select organs. We hypothesized that one active CLA isomer was responsible for the reduced prostaglandin release and that the mechanism was through the inhibition of inducible cyclooxygenase-2 (COX-2). Here, we examined the effects of 10t,12c-CLA and 9c,11t-CLA on COX-2 protein/mRNA expression, prostaglandin E(2) (PGE(2)) production, and the mechanism by which CLA affects COX-2 expression and prostaglandin release. The COX-2 protein expression level was inhibited 80% by 10t, 12c-CLA and 26% by 9c,11t-CLA at 100 microM in vitro. PGE(2) production was decreased from 5.39 to 1.12 ng/2 x 10(6) cells by 10t,12c-CLA and from 5.7 to 4.5 ng/2 x 10(6) cells by 9c,11t-CLA at 100 microM. Mice fed 10t,12c-CLA but not 9c,11t-CLA were found to have a 34% decrease in COX-2 protein and a 43% reduction of PGE(2) release in the lung. 10t,12c-CLA reduced COX-2 mRNA expression level by 30% at 100 microM in vitro and by 30% in mouse lung in vivo. Reduced COX-2 mRNA was attributable to an inhibition of the nuclear factor kappaB (NF-kappaB) pathway by 10t,12c-CLA. These data suggested that the inhibition of NF-kappaB was one of the mechanisms for the reduced COX-2 expression and PGE(2) release by 10t,12c-CLA.
Animals↗
Contribution of rumen protozoa to duodenal flow of nitrogen, conjugated linoleic acid and vaccenic acid in steers fed silages differing in their water-soluble carbohydrate content.
The present experiment was designed to estimate the quantitative contribution of rumen protozoa to the total N, conjugated linoleic acid (CLA) and vaccenic acid (VA; trans-11-18 : 1) flow to the duodenum of steers fed two silage diets: control silage (CS) and silage high in water-soluble carbohydrates (HS). Protozoal duodenal flows were estimated using a real-time PCR assay to quantify the genes encoding protozoal 18S ribosomal RNA. Denaturing gradient gel electrophoresis was used to confirm that the rumen protozoa populations were similar to the protozoal population flowing to the duodenum. Estimated duodenal flow of protozoal N was 14.2 and 18.2 g/d (P>0.05) for animals fed the CS and HS diets respectively. Protozoal flow thus represented between 12 and 15 % of the total N duodenal flow. In terms of fatty acid flow, protozoa accounted for between 30 and 43 % of the CLA and 40 % of the VA reaching the duodenum. The contribution of protozoa to 16 : 0 and 18 : 0 flows to the duodenum was less than 20 and 10 %, respectively. These results show that the fatty acids within protozoa make up a significant proportion of the CLA and VA reaching the duodenum of ruminants.
Animals↗
Prostaglandin formation and platelet aggregation during fasting and linoleic acid intake.
Prostaglandin formation, estimated by the determination of tetranorprostanedioic acid (TNPDA) in the urine, and platelet aggregation were investigated in seven healthy volunteers each day during fasting, and in three of them additionally during intake of carbohydrates (328kcal/day) or safflor oil (328 kcal, 20 g linoleic acid). Monitoring TNPDA in 8-h fractions of the urine showed a reduction during the night (23.00-07.00) by 70% on the average. During Days 1 and 2 of fasting the amount of TNPDA in 24-h urine was the same as under a conventional diet. On Day 3, TNPDA decreased in all experimental subjects to 162 micrograms/day on the average and was not changed by carbohydrate intake. A linoleic acid intake of 20 g/day increased TNPDA in 24-h urine to pre-experimental levels measured under free diet. Platelet aggregation did not change during the experiment. No relationship between prostaglandin formation and lipolysis in man was found.
Adult↗
Conjugated linoleic acid and black currant seed oil in the treatment of canine atopic dermatitis: a preliminary report.
Although conjugated linoleic acid (CLA) shows inhibitory effects on histamine release, eicosanoid production and pruritus in laboratory rodents, its use in canine atopic dermatitis (AD) has not been reported. The aims of this study were to assess the efficacy of CLA, black currant seed oil (BSO) or a combination of both, compared to placebo, in dogs with AD and to evaluate any changes in fatty acid metabolism with these treatments. Twenty-four dogs with AD were randomly allocated to four groups, and were treated orally each day for two months with either 1 mL/10 kg CLA (80% purity), 1 mL/10 kg pure BSO, 1 mL/10 kg CLA+1 mL/10 kg BSO, or 1 mL/10 kg sugar syrup (placebo). Serum was obtained on days 0, 30 and 60 for analysis of CLA metabolites, linoleic acid (LA), gamma-linolenic acid (GLA), dihomo-gamma-linolenic acid (DGLA) and arachidonic acid (AA). At the same time point, the owners were asked to assess pruritus and the veterinarians evaluated any skin lesions present. Although the best clinical results occurred with BSO treatment alone, improvement of clinical signs and pruritus was not significant with any of the treatments. Serum levels of GLA and DGLA significantly increased in BSO-treated dogs, but not in the CLA+BSO group. CLA at the dosage used in this study was not efficacious in treating canine AD, whereas BSO may help some dogs with AD, although further studies are necessary before this can be recommended as a treatment.
Animals↗
EFFECTS OF PALMITIC, OLEIC, AND LINOLEIC ACIDS ON HEPATIC AND VASCULAR LIPID DEPOSITS.
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Cholesterol↗