Conjugated linoleic acid supplementation modified the body composition and serum leptin levels in weaning rats

Dietary supplementation with conjugated linoleic acid (CLA) may reduce body fat mass and increase lean body mass in various species. The objective of this study was to study the effects of conjugated linoleic acid (CLA) supplementation on body composition, serum leptin and triacylglycerol levels in Wistar rats. Rats received linoleic acid (group C) or conjugated linoleic acid (group AE, supplemented with AdvantEdge CLA, and group CO, supplemented with CLA One) in the concentrations of 2% of daily feed consumption. Serum leptin and triacylglycerol levels of rats were measured by means of commercial kits. After 42 days of supplementation, rats in the control group exhibited body fat contents of 53.94 +/- 6.80 g, and those in groups AE and CO had 45.43 +/- 4.86 g and 43.75 +/- 1.93 g, respectively, corresponding to a mean body fat reduction of 18%. Water, whole body protein and ash contents of rats supplemented with CLA were statistically higher relative to control group content (corresponding to a mean increasing of 7.65%; 6.5% and 12.35%, respectively). Experimental groups AE and CO, which received CLA supplementation, had statistically lower serum leptin levels (3.45 +/- 0.46 ng/mL and 3.08 +/- 0.19 ng/mL, respectively) relative to the control group (4.21 +/- 0.22 ng/mL) which received linoleic acid. Triacylglycerol levels did not change after CLA supplementation (p > 0.05). Supplementation with conjugated linoleic acid in the concentration of 2% of mean daily feed consumption was able to change body composition of rats after 42 days of experimentation.     

Conversion of allylic hydroxy oleate to conjugated linoleic acid and methoxy oleate by acid-catalyzed methylation procedures

Conjugated linoleic acid (CLA), a term describing a group of conjugated octadecadienoic acids that are both naturally occurring and formed during food processing, is the subject of considerable current research because of the recently reported antioxidant and anticarcinogenic properties of these compounds. Allylic hydroxy oleates (AHOs), secondary products of lipid autoxidation, have also been found in foods. By means of high-performance liquid chromatography with ultraviolet detection, gas chromatography/mass spectrometry and gas chromatography/matrix isolation/Fourier transform infrared spectroscopy, we determined that currently used acid-catalyzed methylation procedures convert AHOs to CLA and other products that potentially yield high values in determination of CLA in foods. A mixture of AHOs, containing mainly (8- and 11-)hydroxy-9-octadecadecenoates, was synthesized and tested by methylation procedures with the following catalysts: BF₃, HCl, NaOMe and tetramethylguanidine. Both the BF₃ and the HCl procedures converted AHOs to CLA. The base-catalyzed procedures did not convert AHOs to CLA.     

Oxidative Stability of Polyunsaturated Triacylglycerols Encapsulated in Oleaginous Yeast

Oleaginous yeast cells have the ability to synthesize oil from carbon sources or to adsorb fatty acids from their growth medium. Fish oil or conjugated linoleic acid (CLA)-rich oils encapsulated in Cryptococcus curvatus were protected from oxidation for more than 7 weeks. Oil-containing dead and viable yeast as well as oils extracted from dead or viable yeast were incubated at 52 °C in the dark. Oils extracted from yeast at the beginning of the experiment began oxidizing almost immediately and exceeded peroxide values (PV) of 20 mequiv/kg within a few days and eventually reaching PV > 100 mequiv/kg. After 56 days of incubation the PV value of oil from viable cells grown on fish oil was 3.8 ± 0.1 and 5.5 ± 0.8 mequiv/kg from dead cells. After 42 days of incubation the PV of oil from viable CLA containing yeast was 1.1 ± 0.2 mequiv/kg and 1.7 ± 0.5 from dead CLA containing yeast. C. curvatus encapsulation significantly improved oxidative stability of long-chain polyunsaturated fatty acids (LCPUFA) and CLA. Yeast cell viability was not critical for oxidative stability of the encapsulated oil.     

Oxidation kinetics for <Emphasis Type="Italic">cis</Emphasis>-9,<Emphasis Type="Italic">trans</Emphasis>-11 and <Emphasis Type="Italic">trans</Emphasis>-10,<Emphasis Type="Italic">cis</Emphasis>-12 isomers of CLA

The autoxidation processes of the cis-9,trans-11 (c9,t11) and trans-10,cis-12 (t10,c12) isomers of CLA were separately observed at ca. 0% RH and different temperatures. The t10,c12 CLA oxidized faster than the c9,t11 isomer at all tested temperatures. The first half of the oxidation process of t10,c12 CLA obeyed an autocatalytic-type rate expression, but the latter half followed first-order kinetics. On the other hand, the entire oxidation process of c9,t11 CLA could be expressed by the autocatalytic-type rate expression. The apparent activation energies and frequency factors for the autoxidation of the isomers were estimated from the rate constants obtained at various temperatures based on the Arrhenius equation. The apparent activation energies for the CLA isomers were greater than those for the nonconjugated n−6 and n−3 PUFA or their esters. However, the enthalpyentropy compensation held during the autoxidation of both the CLA and PUFA. This suggested that the autoxidation mechanisms for the CLA and PUFA were essentially the same.     

Oxidation of Corn Oils with Spiked Tocols

Stripped corn oils with added tocopherols and tocotrienols, at concentrations between 100 and 5,000 ppm, were used to evaluate antioxidant activity of these tocol compounds. The formation of lipid hydroperoxides, measured as peroxide value (PV), was accelerated at 60 °C in the dark for 5 days. Resistance to oxidation as induction period (IP) was also measured using an oxidative stability instrument (OSI) at 100 °C. For PV inhibition, the oils containing α-tocols exhibited decreasing effectiveness with increasing concentration. At day five, samples with 100 ppm α-tocols had the lowest PVs of about 40 mequiv/kg and samples containing 5,000 ppm had the highest values, ranging from 150 to 200 mequiv/kg. At concentrations above 700 ppm of α-tocols, there was an inversion of antioxidative properties as α-tocols promoted lipid oxidation. The opposite concentration effect was observed with δ-tocols and γ-tocotrienol (T3) for which antioxidant effectiveness increased with concentration. OSI-IP hour at 100 °C increased with increasing tocol concentrations for all tocol homologs, although with diminishing effectiveness at greater than 700 ppm. The α-tocols were less effective in extending the IP (~9 h at 5,000 ppm) than the δ-tocols and γ-T3 (13–14 h at 5,000 ppm). Therefore, the antioxidant or prooxidant activities of different tocols are different and the outcomes are different depending on the evaluation methods used.     

Rosiglitazone,a PPAR-γ Agonist,Fails to Attenuate CLA-Induced Milk Fat Depression and Hepatic Lipid Accumulation in Lactating Mice

Our objective was to investigate the combination of rosiglitazone (ROSI) and conjugated linoleic acid (CLA) on mammary and hepatic lipogenesis in lactating C57Bl/6 J mice. Twenty-four lactating mice were randomly assigned to one of four treatments applied from postpartum day 6 to day 10. Treatments included: (1) control diet, (2) control plus 1.5 % dietary CLA (CLA) substituted for soybean oil, (3) control plus daily intra-peritoneal (IP) rosiglitazone injections (10 mg/kg body weight) (ROSI), and (4) CLA plus ROSI (CLA-ROSI). Dam food intake and milk fat concentration were depressed with CLA. However, no effects were observed with ROSI. The CLA-induced milk fat depression was due to reduced expression for mammary lipogenic genes involved in de-novo fatty acid (FA) synthesis, FA uptake and desaturation, and triacyglycerol synthesis. Liver weight (g/100 g body weight) was increased by CLA due to an increase in lipid accumulation triggering a compensatory reduction in mRNA abundance of hepatic lipogenic enzymes, including acetyl-CoA carboxylase I and stearoyl-CoA desaturase I. On the contrary, no effects were observed with ROSI on hepatic and mammary lipogenic gene and enzyme expression. Overall, feeding CLA to lactating mice induced milk fat depression and increased hepatic lipid accumulation, probably due to the presence of trans-10, cis-12 CLA isomer, while ROSI failed to significantly attenuate both hepatic steatosis and reduction in milk fat content.     

Effects of tocopherols and tocotrienols on the inhibition of autoxidation of conjugated linoleic acid

The effect of eight vitamin E homologues, i.e. α‐, β‐, γ‐, and δ‐tocopherol and α‐, β‐, γ, and δ‐tocotrienol, on the inhibition of autoxidation of conjugated linoleic acid (CLA) were investigated. The oxidation was carried out in the dark for 21 days at 50 °C and monitored by peroxide values (PV) and TBA values. The levels of the individual vitamin E homologues in CLA during storage were determined by HPLC. γ‐Tocopherol exhibited the highest antioxidant activity among the homologues tested in this study when the antioxidant activities of the individual homologues in CLA were compared by PV. The order of antioxidant activity of eight homologues was γ‐tocopherol > δ‐tocopherol = δ‐tocotrienol ≥ γ‐tocotrienol > β‐tocopherol = β‐tocotrienol > α‐tocopherol = α‐tocotrienol. The degradation rates of α‐tocopherol and α‐tocotrienol were faster than those of the other homologues, whereas δ‐tocopherol had the highest stability in CLA during storage. All homologues exhibited an antioxidant activity by inhibiting the formation of secondary oxidation products. It appears that α‐tocotrienol and β‐tocotrienol have significantly higher antioxidant activities for secondary oxidation in CLA than α‐tocopherol and β‐tocopherol. Meanwhile, the other homologues, namely γ‐tocopherol, γ‐tocotrienol, δ‐tocopherol, and δ‐tocotrienol, exhibited similar antioxidant activity for secondary oxidation in CLA.     

Effect of some terpenyl oleates on soybean oil oxidation at 180°C

The ability of linalyl oleate (LO) to act as an autoxidation inhibitor in soybean oil at 180±5°C was compared with the oleates of geraniol (GeO), menthol (MenO), perillyl alcohol (PeO), farnesol (Fa)), phytol (PhO), and cholesterol (ChO) at levels of 0.1% by weight in the oil. Changes in FA composition and conjugated dienes were monitored. Logarithmic plots of the decreasing ratios of linoleate/palmitate and linolenate/palmitate vs. time were linear for soybean oil controls, but plots for LO, GeO, MenO, PeO, FaO, and ChO had inflection points (IP) at times between 5 and 11.4 h. These terpenyl oleates had smaller rate constants before the IP than the control oil. Thus, these esters all exhibited autoxidation inhibition, which was confirmed by conjugated diene values. Plots for PhO had no IP and very limited inhibitory effect relative to the controls. LO originally was chosen for study because it has a double bound structure similar to that of the side chain of avenasterol, which also shows an ability to inhibit oxidation. The ability of terpenyl oleates having widely different structures to inhibit autoxidation suggests that LO's double bound structure is not the cause of its inhibitory activity.     

The Synergism of Biochemical Components Controlling Lipid Oxidation in Lamb Muscle

Lipid oxidation of M. longissimus lumborum in fresh or vacuum packaged (aged) lamb meat stored at 3 °C for 0 or 4 weeks, respectively and displayed under refrigerated conditions for a further 4 days was assessed by measuring the concentration of malondialdehyde (MDA) in meat using the thiobarbituric acid reactive substances procedure. The effects of vitamin E, heme iron and polyunsaturated fatty acids (n-6 and n-3) on lipid oxidation were examined. Results showed a strong positive relationship between heme iron, n-6 and n-3 fatty acids and lipid oxidation when vitamin E was below 2.95 mg/kg muscle. When lipid oxidation was related to vitamin E concentration and the other three variables, respectively, any increase in heme iron or n-6 or n-3 fatty acids concentration did not influence lipid oxidation. Management of diet to elevate muscle vitamin E concentration above 3.45 mg/kg muscle is beneficial to maintain the level of lipid oxidation below 2.4 mg MDA/kg muscle in meat stored for up to 4 weeks. This demonstrates that vitamin E concentration in muscle has a greater influence on controlling lipid oxidation in muscle tissues than do heme iron or polyunsaturated fatty acids.     

Conjugated Linoleic Acid Induces Uncoupling Protein 1 in White Adipose Tissue of <Emphasis Type="Italic">ob/ob</Emphasis> Mice

Conjugated linoleic acid (CLA) reduces body weight and adipose mass in a variety of species. The mechanisms by which CLA depletes adipose mass are unclear, but two independent microarray analyses indicate that in white adipose tissue (WAT), uncoupling protein 1 (UCP1) was among genes most changed by CLA. The objective of this study was to determine whether CLA induces ectopic expression of UCP1 in WAT, which may contribute to increased energy expenditure and weight loss. Six-week old, male ob/ob mice were fed either a control diet (CON) or a diet supplemented with 1.5% mixed isomer CLA (CLA) for 4 weeks. A third group of mice (LEPTIN) was fed the control diet and received daily injections of recombinant leptin as a positive control for adipose depletion in ob/ob mice. CLA did not alter several mRNA markers of lipid oxidation in epididymal white adipose tissue (eWAT) , but significantly increased carnitine palmitoyltransferase-1b (CPT1b) and PPAR gamma coactivator-1α (PGC1α) expression. Notably, CLA increased both mRNA and protein expression of uncoupling protein-1 (UCP1). β3-adrenoceptor mRNA and phosphorylated-p38 mitogen activated protein kinase (MAPK) protein levels were not affected by CLA, but were upregulated by LEPTIN. These data suggest the increased CPT1b, PGC1α, and UCP1, in WAT of CLA-fed mice may contribute to the depletion of adipose, and CLA does not appear to increase UCP1 through β3-adrenergic signaling. Future studies will focus on understanding how CLA increases mitochondrial oxidation and energy dissipation in white adipose tissue.     

Shelf‐life prediction of perilla oil by considering the induction period of lipid oxidation

Kinetic models for the induction period (IP) of lipid oxidation were developed to predict the shelf‐life of perilla oil during storage. The degree of lipid oxidation was measured in terms of peroxide values (PV). The perilla oil was stored in the dark at various temperatures. The IP was measured at the intersection point of two linear lines and in terms of time and PV at the IP. The IP was expressed by an Arrhenius‐like relationship. Before and after the IP, the reaction followed pseudo‐zero‐order kinetics. The oxidation degrees according to storage times were computed by considering the variables, IP and reaction rate constants. The prediction model equation that was developed to determine shelf‐life is more accurate than in previous studies. Conclusively, considering the IP of lipid oxidation is essential for predicting the shelf‐life of perilla oil and is expected to be applicable to other vegetable oils. Practical applications : In kinetic modeling for shelf‐life estimation in terms of lipid oxidation, induction period (IP) is rarely considered. Thus the estimation of peroxide values (PV) from such models might be inaccurate. The IP was observed in perilla oil oxidation and kinetic models involving the IP were developed. This work enables a better estimation of oxidation. Besides, a shelf‐life diagram of perilla oil has been constructed as a valuable tool for quality control in the food industry.     

Conjugated linoleic acid reduces hepatic steatosis, improves liver function, and favorably modifies lipid metabolism in obese insulin-resistant rats

CLA has been shown to induce or suppress excess liver lipid accumulation in various animal models. Interestingly, the state of insulin resistance may be an important modulator of this effect. The objective of the current study was to determine how feeding a dietary CLA mixture would affect liver lipid accumulation in insulin-resistant/obese and lean rats in relation to liver function, lipidemia, liver TAG and phospholipid FA composition, and expression of hepatic markers of FA transport, oxidation, and synthesis. Six-week-old fa/fa and lean Zucker rats (n=20/genotype) were fed either a 1.5% CLA mixture or a control diet for 8 wk. CLA supplementation reduced liver lipid concentration of fa/fa rats by 62% in concurrence with improved liver function (lower serum alanine aminotransferase and alkaline phosphatase) and favorable modification of the serum lipoprotein profile (reduced VLDL and LDL and elevated HDL) compared with control-fed fa/fa rats. The fa/fa genotype had two-thirds the amount of CLA (as % total FA) incorporated into liver TAG and phospholipids compared with the lean genotype. In both genotypes, CLA altered the hepatic FA profile (TAG greater than phospholipids) and these changes were explained by a desaturase enzyme index. Liver-FA-binding protein and acyl CoA oxidase, markers of FA transport and oxidation, respectively, were expressed at higher levels in CLA-fed fa/fa rats. In summary, these results illustrate a strong relationship between the state of insulin resistance and liver lipid metabolism and suggest that CLA acts to favorably modify lipid metabolism in fa/fa Zucker rats.     

Effects of cis-9,trans-11 CLA in rats at intake levels reported for breast-fed infants

CLA intake in exclusively breast-fed infants is close to levels found to have physiological effects in animals. However, in the majority of studies mixtures of CLA isomers have been used and the independent effects of the major CLA isomer in human milk, cis-9, trans-11 CLA, at the intake level in exclusively breast-fed infants have hardly been studied. We therefore studied the effects of cis-9, trans-11 CLA on plasma lipids and glucose, immune function, and bone metabolism in growing rats. Thirty male Sprague-Dawley rats (n=10/group) were fed either 20 mg/kg/d cis-9, trans-11 CLA and 20 mg/kg/d sunflower oil (CLA20), 40 mg/kg/d cis-9, trans-11 CLA (CLA40), or 40 mg/kg/d sunflower oil (placebo) for 8 wk. No significant differences between groups were found in plasma lipids, glucose, insulin, C-reactive protein, or lipid peroxidation. Liver fat content was lowest in the CLA20 group. In vitro interleukin 2 (IL-2) production increased, and tumor necrosis factor alpha, IL-1β, prostaglandin E₂, and leukotriene B₄ production decreased in the CLA20 group. No differences between groups were detected in IL-4, IL-6, or interferon gamma production, plasma osteocalcin, insulin-like growth factor, or urinary deoxypyridino line crosslinks. Plasma tartrate-resistant acid phosphatase 5b activity was significantly increased in the CLA40 group. The results indicate anti-inflammatory effects and enhanced T-cell function for the CLA20 group. No adverse effects were seen in the CLA20 group, whereas indications of increased bone resorption rate were observed in the CLA40 group.     

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 μM efficiently inhibited PLPC oxidation, as evident from a clear lagphase. In contrast, 0.75 μM 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 μM/0.05–20 μM), both vitamin E (1 μM) and ethylene glycol-bis(aminoethyl ether) tetraacetic acid (50 μM) efficiently inhibited PLPC oxidation. However, CLA (1–50 μM) 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.     

The effect of conjugated linoleic acid on the antioxidant enzyme defense system in rat hepatocytes

Short-term effects of physiological concentrations of conjugated linoleic acid (CLA) on membrane integrity, metabolic function, cellular lipid composition, lipid peroxidation, and antioxidant enzymes were examined using rat hepatocyte suspension cultures. Incubation with CLA (5–20 ppm) for 3 h decreased the ability of hepatocyte plasma membranes to exclude trypan blue by approximately 25%, and caused leakage of cytosolic lactate dehydrogenase (LDH) into the medium. The significant decrease (P<0.02) in hepatocyte viability as measured by LDH leakage during cell incubation with 10 and 20 ppm CLA was not associated with significant changes in cellular ATP content. Protein synthesis in hepatocytes was elevated (P<0.05) in the presence of 5 and 10 ppm CLA, but at a higher concentration (20 ppm), protein synthesis was similar to that of control cells. Gluconeogenesis was maintained in cells incubated with lower concentrations of CLA (5 and 10 ppm) but was decreased (P<0.02) at the higher concentration. Incubation with 20 ppm CLA for 3 h did not affect the specific activity of 3-hydroxy-3-methylglutaryl coenzyme A reductase, the rate-limiting enzyme of cholesterol synthesis. Both cis-9,trans-11/trans-9,cis-11, and cis-10,trans-12/trans-10,cis-12 isomers of CLA were incorporated to a similar level into hepatocytes. Levels ranged from 3.9 to 4.1%, respectively, of total fatty acids in neutral lipids, and from 0.7 to 0.8%, respectively, of total fatty acids in phospholipids. Cellular lipid peroxidation remained unchanged in the presence of CLA (5–20 ppm), despite significant inhibition (P<0.05) of superoxide dismutase. Catalase activity was maintained near control levels in the presence of 5 and 10 ppm CLA but was significantly decreased in the presence of 20 ppm CLA. Glutathione peroxidase activity was significantly decreased in the presence of 10 ppm CLA. The apparent sensitivity of the antioxidant enzyme defense system of liver cells to CLA, coupled with the lack of effect of CLA on lipid peroxidation in cells, suggests that cytotoxic effects of CLA as described by LDH leakage and decreased gluconeogenesis were not mediated by a prooxidant action in hepatocytes.     

Autoxidation rates of 5-olefinic monoenoic and denoic fatty acids from sea urchin lipids and meadoefoam oils

Autoxidation rates of the 5-olefinic monoenoic and dienoic fatty acids from sea urchin lipids and meadow-foam oils were compared with those of normal monoenoic and dienoic fatty acids by gas-liquid Chromatographic determination of the unoxidized fatty acid methyl esters remaining through the autoxidation period. The fatty acids are classified into five groups shown below according to the oxidation rate of their methyl esters: I 5-olefinic monoenoic acids (c5-18:l, c5-20:l and c5-22:1), II normal monoenoic acids (c9-18:l, cll-18:l, c9-20:1, cl3-20:l and cl3-22:l), III 5-olefinic dienoic acids (c5,cll-20:2, c5,cl3-20:2 and c5,cl3-22:2), IV 7-olefinic dienoic acids (c7,cl3-22:2 and c7,cl5-22:2) and V normal dienoic acids (c6,c9-18:2, c9,cl2-18:2 and cll,cl4-20:2). The oxidation rates of these groups increased during autoxidation in order from I to V. These results show that the 5-olefinic monoenoic and dienoic acids are more stable to autoxidation than the normal monoenoic and dienoic acids, respectively. The higher stabilities of the 5-olefinic monoenoic and dienoic acids in organisms are shown from these results.     

Effects of specific conjugated linoleic acid isomers on growth characteristics in obese Zucker rats

Growing female obese Zucker (fa/fa) rats were treated (via intragastric gavage) for 21 d with either a (i) vehicle [corn oil; 0.9 g/kg body weight (BW)], (ii) CLA mixture [50∶50; trans-10,cis-12 and cis-9,trans-11 CLA], (iii) cis-9,trans-11 CLA, or (iv) trans-10,cis-12 CLA (CLA treatments at 1.5 g CLA/kg BW). Compared with controls, average daily gain (g/d) was reduced 24 and 44% by the CLA mixture and trans-10,cis-12 CLA, respectively There was no treatment effect on average whole-body (minus heart and liver) composition (dry matter basis): fat (70.2%), protein (21.0%), and ash (4.3%). Compared with animals treated with cis-9,trans-11 CLA, obese Zucker rats treated with trans-10,cis-12 and the CLA mixture had 7.8% more carcass water. Treatment had no effect on heart or liver weights or on heart or liver weights as a percentage of body weight, but compared with the other treatments trans-10,cis-12 CLA increased liver lipid contentby 33%. Hepatic lipid ratios of 16∶1/16∶0 and 18∶1/18∶0 (a proxy for Δ⁹-desaturase capability) were not affected by treatment (0.1 and 0.6, respectively). Simlar to previous reports, CLA increased hepatic lipid content and altered both liver and carcass FA composition (i.e., reduced arachidonic acid content), but the ability of CLA to manipulate body composition in obese Zucker rats remains questionable.     

Conjugated linoleic acid supplementation in humans--metabolic effects

Supplementation with conjugated linoleic acid (CLA) induces a number of physiological effects in experimental animals, including reduced body fat content, decreased aortic lipid deposition, and improved serum lipid profile. Controlled trials on the effects of CLA in humans have hitherto been scarce. The aim of this study was to evaluate the effects of supplementation with CLA in healthy humans on anthropometric and metabolic variables and on the fatty acid composition of serum lipids and thrombocytes. Fifty-three healthy men and women, aged 23–63 yr, were randomly assigned to supplementation with CLA (4.2 g/d) or the same amount of olive oil during 12 wk in a double-blind fashion. The proportion of body fat decreased (−3.8%, P<0.001) in the CLA-treated group, with a significant difference from the control group (P=0.050). Body weight, body mass index, and sagittal abdominal diameter were unchanged. There were no major differences between the groups in serum lipoproteins, nonesterified fatty acids, plasma insulin, blood glucose, or plasminogen activator inhibitor 1 (PAI-1). In the CLA group the proportions of stearic, docosatetraenoic, and docosapentaenoic acids increased in serum lipids and thrombocytes, while proportions of palmitic, oleic, and dihomoγ-linolenic acids decreased, causing a decrease of the estimated Δ-6 and Δ-9 and an increase in the Δ-5 desaturase activities. These results suggest that supplementation with CLA may reduce the proportion of body fat in humans and that CLA affects fatty acid metabolism. No effects on body weight, serum lipids, glucose metabolism, or PAI-1 were seen.     

Response of urinary malondialdehyde to factors that stimulate lipid peroxidation in vivo

Malondialdehyde (MDA) derivatives occur as normal constituents of rat and human urine. In a previous study, it was found that MDA excretion in rats is responsive to MDA intake and to certain factors that increase lipid peroxidation in vivo: vitamin E deficiency, iron administration and a high concentration of cod liver oil (CLO) fatty acids in the tissues. In the present study, the effect on MDA excretion of several additional dietary and endogeneous factors was evaluated. The composition of dietary fatty acids had a major influence on MDA excretion in fed animals, being highest for animals fed n−3 fatty acids (20∶5 and 22∶6) from CLO, intermediate for those fed n−6 (18∶2) acids from corn oil (CO) and lowest for those fed saturated acids from hydrogenated coconut oil (HCO). Diet was the main source of urinary MDA in all groups. Fasting produced a marked increase in urinary MDA, which tended to be higher in rats previously fed CLO. Fasting MDA excretion was not affected by the level of CO in the diet (5, 10 or 15%), indicating that feeding n−6 acids does not increase lipid peroxidation in vivo. Adrenocorticotropic hormone and epinephrine administration increased urinary MDA, further indicating that lipolysis either releases fatty acid peroxides from the tissues or increases the susceptibility of mobilized fatty acids to peroxidation. A decrease in fasting MDA excretion was observed in rats previously fed a high level of antioxidants (vitamin E+BHT+vitamin C) vs a normal level of vitamin E. MDA excretion increased following adriamycin and CCl₄ administration. No increase was observed following short-term feeding of a choline-methionine-deficient diet, which has been reported to increase peroxidation of rat liver nuclear lipids. This study provides further evidience that urinary MDA can serve as a useful indicator of lipid peroxidation in vivo when peroxidation of dietary lipids is precluded. This research was performed in partial fulfillment of the requirements for the M.Sc. degree in Nutritional Sciences