Dietary CLA Research Articles

Effects of dietary supplementation of different oils and conjugated linoleic acid on the reproductive and metabolic aspects of male mice.

The present study was carried out to examine first, if diets enriched with 320 g of the base diet with common dietary oils including fish oil, olive oil, hydrogenated sunflower seed (H-SFS) oil, flaxseed oil and sunflower seed oil (SFS) could induce weight gain and alter reproductive and metabolic characteristics of male mice. Second, whether the addition of conjugated linoleic acid (CLA, 10% of the diet) could ameliorate any negative effects. In this cross-sectional study, 90 four-week-old male NMRI mice were used in two consecutive experiments. A high level of dietary oils negatively affected some reproductive and metabolic characteristics of male mice (p < 0.05), specifically, sunflower seed oil enrichment resulted in higher HDL levels and apoptosis of germinal epithelial cells. An olive oil-enriched diet caused an increase in plasma triglyceride concentrations and germinal cell apoptosis, as well as a decrease in sperm concentration and perturbed spermatogenesis. When CLA was fed in conjunction with dietary oils it successfully mitigated some of the negative reproductive and metabolic characteristics. We conclude that male reproductive processes are affected by high dietary oils, even before signs of obesity are evident. Inclusion of dietary CLA may provide some benefit to offset negative effects, although further studies are required.

Evaluation of conjugated linoleic acid supplementation on markers of joint inflammation and cartilage metabolism in young horses challenged with lipopolysaccharide.

Seventeen yearling Quarter Horses were used in a randomized complete block design for a 56-d trial to determine ability of dietary CLA to mitigate joint inflammation and alter cartilage turnover following an inflammatory insult. Horses were blocked by age, sex, and BW, and randomly assigned to dietary treatments consisting of commercial concentrate offered at 1% BW (as-fed) supplemented with either 1% soybean oil (CON; n = 6), 0.5% soybean oil and 0.5% CLA (LOW; n = 5; 55% purity; Lutalin, BASF Corp., Florham Park, NJ), or 1% CLA (HIGH; n = 6) top-dressed daily. Horses were fed individually every 12 h and offered 1% BW (as-fed) coastal bermudagrass (Cynodon dactylon) hay daily. This study was performed in 2 phases: phase I (d 0 to d 41) determined incorporation of CLA into plasma and synovial fluid; phase II (d 42 to d 56) evaluated potential of CLA to mitigate intra-articular inflammation and alter cartilage metabolism. Blood and synovial fluid were collected at 7- and 14-d intervals, respectively, to determine fatty acid concentrations. On d 42, carpal joints within each horse were randomly assigned to receive intra-articular injections of 0.5 ng lipopolysaccharide (LPS) derived from Escherichia coli 055:B5 or sterile lactated Ringer's solution. Synovial fluid samples were obtained at preinjection h 0 and 6, 12, 24, 168, and 336 h postinjection, and analyzed for prostaglandin E2 (PGE2), carboxypeptide of type II collagen (CPII), and collagenase cleavage neopeptide (C2C). Data were analyzed using PROC MIXED procedure of SAS. Horses receiving the CON diet had undetectable levels of CLA for the duration of the study. A quadratic dose response was observed in concentrations of CLA in plasma and synovial fluid (P < 0.01). A negative quadratic dose response was observed for plasma arachidonic acid (20:4) with a reduction in concentration to d 14 in HIGH horses (P = 0.04). Synovial fluid 20:4 tended to decrease in horses receiving the HIGH diet (P = 0.06). Post LPS injection, synovial PGE2 was not affected by dietary treatment (P = 0.15). Synovial C2C was lower in HIGH horses (P = 0.05), and synovial CPII tended to be greater in LOW horses than HIGH and CON horses (P = 0.10). In conclusion, dietary CLA incorporated into plasma and synovial fluid prior to LPS challenge. Dietary CLA did not influence inflammation; however, there was a reduction in cartilage degradation and an increase in cartilage regeneration.

Chromium, CLA, and ractopamine for finishing pigs.

This study aimed to evaluate the effects of dietary chromium, CLA, and ractopamine on performance, carcass traits, and pork quality of finishing pigs slaughtered at 115 kg BW. Ninety-six crossbred barrows (initial BW = 70.21 ± 1.98 kg) were randomly assigned to 1 of 6 dietary treatments. There were 8 replicates per treatment (48 pens; 2 pigs/pen). A diet formulated according to the nutritional requirements was used as the control (CON). The other 5 diets were based on the CON and supplemented as follows: 0.4 mg/kg Cr yeast (CrY); 0.5% CLA; 0.4 mg/kg CrY and 0.5% CLA (CrY + CLA); 20 mg/kg ractopamine (RAC); 0.4 mg/kg CrY and 20 mg/kg RAC (CrY + RAC). Lysine levels on diets containing ractopamine were raised by 20% compared to CON to meet the greater requirements of pigs fed ractopamine. Pigs fed RAC and CrY + RAC were fed CON for the first 17 d, and then the respective diets for the last 28 d on trial. Data were analyzed in a model including the fixed effect of treatment (6 levels) and initial BW as a covariate for all characteristics, with the exception of carcass traits, in which final BW was used as a covariate. Least-squares means were separated using Tukey-Kramer's method. Differences were considered when probability values were lower than 0.05. Pigs fed RAC and CrY + RAC had the greatest ( < 0.001) final BW and ADG. Pigs fed CrY + RAC had greater ( < 0.001) G:F than pigs within the other groups, except for those fed RAC. Pigs fed CrY + RAC and RAC had similar G:F, both greater ( < 0.001) than pigs fed CON. Average daily feed intake was similar ( = 0.83) for all diets. Pigs fed CrY + RAC had greater LM area ( = 0.01) and carcass yield ( < 0.02) than pigs fed CON, CrY, CLA, and CrY + CLA. Loin muscle area and carcass yield of pigs fed RAC were not different from pigs fed the others diets. Pigs fed CON diets had greater BF ( = 0.02) than pigs fed CLA diet. Additives did not affect ( > 0.05) pork quality, except for color. No differences ( > 0.05) were observed for carcasses pH and temperature. The values for pigs fed RAC were greater ( = 0.01) than pigs fed other diets. Pigs fed RAC had lower ( < 0.01) values compared to pigs fed other experimental diets. Serum urea nitrogen concentration (SUN) was lower ( = 0.02) in pigs fed CrY + RAC than in pigs fed CON and RAC and similar to pigs fed the other feeding additives. In summary, it was demonstrated that, when combined, CrY and RAC increase LM area and carcass yield, and reduce SUN, suggesting that chromium could improve nutrient utilization by muscle cells in RAC-fed pigs. Additionally, the additives have no major effects on pork quality.

708 Influence of conjugated linoleic acid supplementation on body composition of growing pigs

Thirty-two crossbred gilts (8 wk and 15.9 kg) of similar breeding were used in a randomized complete block design to evaluate the effects of dietary supplementation of CLA on body composition of young, growing pigs. Pigs were blocked by BW and randomly assigned and evenly distributed among 3 treatment groups or a control group for an 84-d feeding trial. Diets consisted of a commercially available concentrate (Nutrena, Minneapolis, MN) with CLA supplemented at the rate of 0.33, 0.66, or 1.0% of the diet. The CLA source (BASF Corp., Florham Park, NJ) contained 55% CLA (mixture of cis-9, trans-11; trans-10, cis-12; and trans-9, trans-11 isomers). The control group received the same pelleted concentrate in addition to soybean oil supplemented at 0.33% of the total diet. Oil was administered as a drench to the control group and all treatment groups at 0600 h daily to ensure consumption. Body weight was obtained every 7 d with the intake of concentrate and supplement was adjusted accordingly. Fat thickness (cm) was measured at 14-d intervals via ultrasonography at the 10th rib, and LM area (LMA) was collected via ultrasonography at d 0, 42, and 84. Data were analyzed using the MIXED procedure of SAS. Overall effects were analyzed using repeated measures, and data from individual days were analyzed using fat thickness from d 0 as a covariate. Overall, there was no difference between treatments in BW (P = 0.74), 10th-rib fat thickness (P = 0.36), or LMA (P = 0.70). There was a significant treatment × time interaction for fat thickness. Tenth-rib fat thickness was lower at d 70 (P < 0.03) and 84 (P < 0.04) for pigs consuming 0.66 and 1.0% CLA compared with the control group. These data indicate that CLA supplemented at 0.66 or 1.0% of the diet fed to young, growing pigs has no effect on BW or LMA but did result in a decrease in back fat thickness after d 70 of treatment. It is likely that this trend would continue if the feeding period had been extended; however, further studies are needed to fully elucidate dietary CLA supplementation to alter body composition when fed to young, growing pigs.

Dietary Docosahexaenoic Acid and trans-10, cis-12-Conjugated Linoleic Acid Differentially Alter Oxylipin Profiles in Mouse Periuterine Adipose Tissue.

Diets containing high n-3 polyunsaturated fatty acids (PUFA) decrease inflammation and the incidence of chronic diseases including cardiovascular disease and nonalcoholic fatty liver disease while trans-fatty acids (TFA) intake increases the incidence of these conditions. Some health benefits of n-3 PUFA are mediated through the impact of their oxygenated metabolites, i.e. oxylipins. The TFA, trans-10, cis-12-conjugated linoleic acid (CLA; 18:2n-6) is associated with adipose tissue (AT) inflammation, oxidative stress, and wasting. We examined the impact of a 4-week feeding of 0, 0.5, and 1.5% docosahexaenoic acid (DHA; 22:6n-3) in the presence and absence of 0.5% CLA on AT oxylipin profiles in female C57BL/6N mice. Esterified oxylipins in AT derived from linoleic acid (LNA), alpha-linolenic acid (ALA), arachidonic acid (ARA), eicosapentaenoic acid (EPA), DHA, and putative from CLA were quantified. CLA containing diets reduced AT mass by~62%. Compared with the control diet, the DHA diet elevated concentrations of EPA-and DHA-derived alcohols and epoxides and LNA-derived alcohols, reduced ARA-derived alcohols, ketones, epoxides, and 6-keto-prostaglandin (PG) F1α (P<0.05), and had mixed effects on ALA-derived alcohols. Dietary CLA lowered EPA-, DHA-, and ALA-derived epoxides, ARA-derived ketones and epoxides, and ALA-derived alcohols. While dietary CLA induced variable effects in EPA-, DHA-, and LNA-derived alcohols and LNA-derived ketones, it elevated ARA-derived alcohols and PGF1α, PGF2α, and F2-isoprostanes. DHA counteracted CLA-induced effects in 67, 57, 43, and 29% of total DHA-, ARA-, EPA-, and ALA-derived oxylipins, respectively. Thus, CLA elevated proinflammatory oxylipins while DHA increased anti-inflammatory oxylipins and diminished concentration of CLA-induced pro-inflammatory oxylipins in AT.

MRNA abundance of genes involved in mammary lipogenesis during fish oil- or trans-10,cis-12 CLA-induced milk fat depression in dairy ewes

Milk fat depression (MFD) caused by trans-10,cis-12 18:2 is known to be mediated in cows and ewes by downregulation of mammary lipogenic genes. However, transcriptional mechanisms underlying marine lipid-induced MFD have not been well defined yet and the few available studies in ovine are not consistent. This trial was conducted to directly compare changes in animal performance, milk fatty acid composition, and particularly mammary mRNA abundance of candidate lipogenic genes and transcription factors in response to the inclusion of fish oil or trans-10,cis-12 18:2 in the dairy sheep diet. To meet this objective, 12 lactating Assaf ewes (on average, 64 days in milk, producing 1.72 kg of milk/d with 5.17% of fat) were divided into 3 groups and offered a total mixed ration without supplementation (control) or supplemented with 2.4% dry matter of fish oil (FO treatment) or 1% dry matter of a commercial product rich in trans-10,cis-12 18:2 (CLA treatment) for 39 d. Measurements and samplings were conducted before starting the treatments and at the end of the trial. Milk samples were used for RNA extraction from somatic cells. Feed intake was not affected by lipid supplements, and as designed, reductions in milk fat concentration (-31%) were similar in the 2 treatments, although the unpredicted increase in milk production with FO counteracted the anticipated reduction in milk fat yield. Nevertheless, this did not preclude the detection of FO-induced decreases in the mRNA abundance of candidate lipogenic genes [e.g., acyl-CoA synthetase short-chain family member 2 (ACSS2), fatty acid synthase (FASN), and lipin 1 (LPIN1)], thus supporting the hypothesis that transcriptional regulation would be a relevant component of this type of MFD in sheep. Expected CLA-induced downregulation of some genes, such as FASN or sterol regulatory element binding transcription factor 1 (SREBF1), could not be detected in our samples, which might be related, at least in part, to high inter-individual variation and relatively advanced lactation stage (on average 102-103 d in milk on d 38 and 39). Overall, direct comparison of the effects of dietary FO and CLA on transcript abundance of candidate lipogenic genes and transcription factors suggest that there might be relevant differences in the transcriptional control mechanisms underlying the MFD induced by each kind of supplement (i.e., fish oil or CLA).

Dose–response relationship in dairy ewes fed a rumen unprotected CLA supplement

Establishment of dose–response relationships between dietary CLA and milk fat inhibition permits to customize CLA supplementation to specific milk fat production targets. The present study evaluated the performance, milk composition, and FA profile of dairy ewes fed 10, 15 or 30g/d of a rumen unprotected CLA supplement and the time course for recovery from milk fat depression. Supplemental lipids consisted of calcium salts of fatty (CSFA) and rumen unprotected CLA methyl ester. Twenty-nine primiparous Lacaune were randomly allotted to 1 of 4 treatments: Control: 30g of CSFA (n=7); CLA1: 20g of CSFA plus 10g of CLA (n=7); CLA2: 10g of CSFA plus 20g of CLA (n=7); and CLA3: 30g of CLA (n=8). The study lasted 35 d (7 d adaptation, 21 d treatment, 7 d recovery). During the recovery period, all animals received the Control treatment. The CLA doses tested did not affect milk yield, milk protein content and secretion, or SCC (P>0.05). Incremental CLA doses reduced milk fat content and secretion in a linear manner. Identical linear response was observed in milk fat concentration of fatty acids ≤C16 (decrease) and >C16 (increase) when CLA dose increased from 0 to 30g/d. The transfer efficiency from diet to milk did not differ between CLA doses (P>0.05). Incremental doses of rumen unprotected CLA methyl ester increased trans-10, cis-12 CLA incorporation into milk fat and the pattern for CLA-induced milk fat decrease was driven by the supply of trans-10, cis-12 CLA to the mammary gland.

Mice do not accumulate muscle lipid in response to dietary conjugated linoleic acid1

Dietary CLA decreases body fat in several species and in pigs this is accompanied by increased muscle lipid. Our objective was to determine if mice could be used as a model for CLA-induced increased marbling in pigs. We used our model of enhanced CLA response, where mice fed coconut oil (CO) lose more body fat than mice fed soy oil (SO). Mice (21 d old; Imprinting Control Region [ICR]) were fed SO or CO diets for 6 wk followed by 12 d of 0 or 0.5% mixed isomer CLA. Ether extraction determined that thigh muscle lipid content was reduced by both CLA and CO (P = 0.007 and P = 0.006, respectively). Conjugated linoleic acid also caused a reduction (P = 0.016) in carnitine palmitoyltransferase (CPT) enzyme activity, so less fatty acid oxidation appeared to be occurring. Lumbar muscle, which is more similar to the longissimus dorsi tested in pigs, did not differ in lipid content between mice (56 d old; ICR) fed SO or SO+CLA for 14 d. Therefore, CLA-fed mice do not appear to be accumulating excess lipid in their muscle. However, CLA addition to CO diets increased (P = 0.007) the mRNA expression of PPAR-γ in the thigh muscle to the level of SO-fed mice, indicating that intramuscular adipocyte differentiation may be increasing. On the other hand, liver lipid was increased (P < 0.0001) by CO and tended to be increased (P = 0.099) by CLA. Liver CPT activity was decreased (P = 0.018) in SO+CLA-fed mice but not CO+CLA. It appears that mice may accumulate lipid in their livers preferentially over muscle when fed CLA and therefore are not a good model for CLA-induced muscle lipid accumulation.

A rumen unprotected conjugated linoleic acid supplement inhibits milk fat synthesis and improves energy balance in lactating goats1

Feeding trans-10, cis-12 CLA supplements in a rumen-protected form has been shown to cause milk fat depression (MFD) in cows, ewes, and goats. Methyl esters of CLA were shown to be as effective as FFA in inducing MFD when infused postruminally, but their efficacy as a feed supplement has not been addressed in studies with lactating ruminants. In the present study, we investigated the effects of an unprotected trans-10, cis-12 CLA supplement as methyl esters on performance, milk composition, and energy status of dairy goats. Eighteen multiparous Toggenburg goats were randomly assigned to dietary treatments in a crossover experimental design (14 d treatment periods separated by a 7 d washout interval): 30 g/d of calcium salts of fatty acids (Control) or 30 g/d of a rumen unprotected CLA supplement containing 29.9% of trans-10, cis-12 CLA as methyl esters (CLA). Lipid supplements were mixed into a concentrate and fed individually to animals 3 times a day as a total mixed ration component. The DMI, milk yield, milk protein and lactose content and secretion, and somatic cell count were unaffected by CLA treatment. On the other hand, milk fat content and yield were reduced by 19.9 and 17.9% in CLA-fed goats. Reduced milk fat yield in CLA-fed goats was a consequence of a lower secretion of both preformed and de novo synthesized fatty acids. The CLA treatment also changed the milk fatty acid profile, which included a reduction in the concentration of SFA (2.5%), increased MUFA and PUFA (5.6 and 5.4%, respectively), and a pronounced increase (1576%) in milk fat trans-10, cis-12 CLA. Consistent with the high milk fat trans-10, cis-12 CLA content, all desaturase indexes were reduced in milk fat from CLA-fed goats. The MFD induced by CLA reduced the energy required for milk production by 22%, which was accompanied by an improvement in the estimated energy balance (P < 0.001), greater blood glucose concentration (P < 0.05), and a trend for increased BW (P = 0.08). Approximately 7.2% of trans-10, cis-12 CLA was estimated to escape from rumen biohydrogenation and indirect comparisons with data obtained from other studies suggest equivalent MFD between dietary CLA in the methyl ester form and rumen protected sources. Thus, despite the apparent low degree of rumen protection, our results suggest that methyl esters of CLA could be an alternative to rumen protected CLA supplements due to manufacturing and cost advantages.

Conjugated linoleic acid (CLA) activates PGC‐1alpha via AMPK and SIRT1 in C2C12 myotubes

Along with its effect on body fat reduction, dietary CLA has been reported to improve physical activity and endurance capacity in mice. It has been suggested these effects are due to up-regulation of skeletal muscle peroxisome proliferator-activated receptor δ (PPARδ), however, the mode of action is not completely understood. Thus, the purpose of the study was to determine the mechanisms of CLA on skeletal muscle PPA Rδ regulation to understand its effects on muscle metabolism. C2C12 myocytes were differentiated into myotubes and effects of CLA (cis-9, trans-11 and trans-10, cis-12) were investigated on major upstream regulators of PPARδ, AMP-activated protein kinase (AMPK), PPAR γ coactivator 1α (PGC-1α), and sirtuin 1 (SIRT1), including time- and dose-dependent effects. Both the cis-9, trans-11 and trans-10, cis-12 CLA isomers significantly increased expressions of AMPK (both total- and phosphorylated-AMPKs), most significantly at 50μM for 12 or 2 4 hour incubation compared to control. However, only the trans-10, cis-12 CLA isomer, but not the cis-9, trans-11 isomer, increased expressions of PGC-1α and SIRT1 (30% and 25%, respectively) compared to control. These results suggest that CLA isomers promote muscle metabolism via AMPK mediated mechanism, where the trans-10, cis-12 CLA isomer is more effective than the cis-9, trans-11 isomer by modulating both AMPK and SIRT1 mediated mechanisms. Grant Funding Source: None

Riboflavin-Photosensitized Oxidation Is Enhanced by Conjugation in Unsaturated Lipids

Methyl esters of polyunsaturated fatty acids were found to quench triplet-excited riboflavin ((3)Rib) in efficient bimolecular reactions with rate constants, as determined by laser flash photolysis, linearly depending upon the number of bis-allylic methylene (from 1 to 5). Deactivation of (3)Rib is predicted by combining the experimental second-order rate constants k2 determined for acetonitrile/water (8:2, v/v) at 25 °C with density functional theory (DFT) calculations of bond dissociation energy to have an upper limiting value of 1.22 × 10(7) L mol(-1) s(-1) for hydrogen abstraction from bis-allylic methylene groups in unsaturated lipid by (3)Rib. Still, ergosterol was found to deactivate (3)Rib with k2 = 6.2 × 10(8) L mol(-1) s(-1), which is more efficient than cholesterol, with 6.9 × 10(7) L mol(-1) s(-1). Likewise conjugated (9E,11E) methyl linoleate (CLA) reacts with 3.3 × 10(7) L mol(-1) s(-1), 30 times more efficient than previously found for methyl α-linolenate. Conjugation as in CLA and ergosterol is concluded to enhance (3)Rib deactivation, and dietary plant sterols and CLA may accordingly be important macronutrients for eye and skin health, protecting against light exposure through efficient deactivation of (3)Rib.

Dietary Conjugated Linoleic Acid Activates PPARγ and the Intestinal Trefoil Factor in SW480 Cells and Mice with Dextran Sulfate Sodium-Induced Colitis1–3

A central event in inflammatory bowel disease is the disruption of the mucosal homeostasis. Trefoil peptides [(TFF)] are emerging as key mediators in the defense and repair of the gastrointestinal mucosa. Here, we demonstrate induction of TFF by CLA with therapeutic antiinflammatory effects in a mouse model of inflammatory bowel disease. SW480 cells were treated with linoleic acid or CLA (0–2.5 μ mol/L) in the absence or presence of the PPARγ inhibitor GW9662. Cells treated with CLA showed an upregulation of the intestinal trefoil factor, which was prevented by pretreatment with GW9662. Dextran sulfate sodium (2%) was used to induce colitis in mice and they were simultaneously fed with a standard or a CLA-supplemented (100 mg · kg -1 · d -1 ) diet for 7 d. The CLA-enriched diet prevented the colon shortening induced by DSS and markedly reduced the disease activity index and the colonic expression of inducible NO synthase and NF-κB. Immunohistochemistry revealed an increase in PPARγ and TFF3 expression after CLA administration. Altogether, these results indicate that dietary CLA protects against DSS-induced colitis in a process involving induction of PPARγ and TFF3.

Effect of corn dried distillers grains with solubles, conjugated linoleic acid, and ractopamine (paylean) on growth performance and fat characteristics of late finishing pigs

An experiment was performed to evaluate effects of dietary ractopamine, CLA, and corn distillers dried grains with solubles (DDGS) on growth and carcass and fat quality of finishing pigs. This study was conducted as a split-split plot arrangement in a generalized randomized block design. In total 1,102 crossbred barrows and gilts (initial BW = 100.4 kg, SD = 3.7 kg; pic 337 × c22) were randomly assigned to 1 of 8 dietary treatments that consisted of 2 diet sources [corn-soybean meal (corn-soy) and corn-soy + 20% DDGS], 2 levels of ractopamine (0 and 7.4 mg/kg), and 2 levels of CLA (0% and 0.6%). The pen was the experimental unit, with 6 replications per treatment for a total of 48 pens with 23 pigs per pen. Pigs had ad libitum access to water and feed during the 27-d experimental period. Ractopamine addition improved (p < 0.05) ADG and G:F over the control group. Furthermore, carcass weight, carcass yield, loin depth, and lean percentage were increased and back fat depth was decreased (p < 0.05) by feeding ractopamine. Feeding CLA resulted in improved (p < 0.05) ADG and G:F and increased lean percentage but reduced carcass yield (p < 0.05). The inclusion of DDGS did not affect ADG, adfi, or g:f but reduced (p < 0.05) carcass dressing percent. An increase (p < 0.05) in the concentration of pufa was observed with inclusion of DDGS, ractopamine, and CLA. Iodine value (iv) increased (p < 0.001) in both belly and jowl samples by feeding DDGS and ractopamine, whereas a decrease (p < 0.01) was observed when CLA was included in the diets. The fatty acid profiles of belly and jowl fat samples were affected (p < 0.05) by diet source × ractopamine, indicating that effects of dietary ractopamine depend on the fatty acid profile of the diet. These results indicate that feeding ractopamine and CLA could improve growth and carcass measures and that CLA was effective in diminishing some of the negative effects, especially on IV, caused by DDGS.

Dietary Intake ofc9,t11-Conjugated Linoleic Acid Correlates with Its Concentration in Plasma Lipid Fractions of Men but Not Women ,

The c9,t11–18:2 isomer of conjugated linoleic acid (c9,t11-CLA) represents the main dietary CLA form with putative health benefits. Whereas CLA intake influences the tissue CLA concentration, little is known about the association between dietary CLA and the CLA content of plasma lipid fractions. This study was designed to document fasting and nonfasting plasma c9,t11-CLA concentrations in a population of free-living adults (n = 94) and relate these concentrations to c9,t11-CLA intake. We also determined the c9,t11-CLA content of the primary plasma lipid fractions in a subset (n = 50) of our participants, related these to c9,t11-CLA intake, and determined whether c9,t11-CLA intake or plasma c9,t11-CLA was correlated with plasma cholesterol. Mean fasting plasma c9,t11-CLA concentrations were 0.46 ± 0.01 and 0.54 ± 0.01% (wt:wt) of total fatty acids for men and women, respectively (P < 0.05); nonfasting concentrations were 0.28 ± 0.01 and 0.38 ± 0.01% of total fatty acids, respectively (P < 0.001). All major esterified plasma lipid fractions contained c9,t11-CLA; TG had the highest percentages. In men, c9,t11-CLA intake correlated (r = 0.47; P < 0.05) with TG c9,t11-CLA content, suggesting that TG c9,t11-CLA may serve as a biomarker for c9,t11-CLA intake. In females, there were no correlations between c9,t11-CLA intake and the c9,t11-CLA content of any esterified plasma lipid fraction. In neither sex was there a relation between dietary c9,t11-CLA or plasma c9,t11-CLA concentration and circulating lipoprotein cholesterol concentration. The influence of sex on circulating c9,t11-CLA content and further validation of biomarkers of c9,t11-CLA intake warrant further investigation.

Examining acute and chronic effects of short- and long-chain fatty acids on peptide YY (PYY) gene expression, cellular storage and secretion in STC-1 cells

Peptide YY (PYY) is a gastrointestinal hormone with physiological actions regulating appetite and energy homoeostasis. The cellular mechanisms by which nutrients stimulate PYY secretion from intestinal enteroendocrine cells are still being elucidated. This study comprehensively evaluated the suitability of intestinal STC-1 cells as an in vitro model of PYY secretion. PYY concentrations (both intracellular and in culture media) with other intestinal peptides (CCK, GLP-1 and GIP) demonstrated that PYY is a prominent product of STC-1 cells. Furthermore, acute and chronic PYY responses to 15 short (SCFAs)- and long-chain (LCFAs) dietary fatty acids were measured alongside parameters for DNA synthesis, cell viability and cytotoxicity. We found STC-1 cells to be reliable secretors of PYY constitutively releasing PYY into cell culture media (but not into non-stimulatory buffer). We demonstrate for the first time that STC-1 cells produce PYY mRNA transcripts; that STC-1 cells produce specific time- and concentration-dependent PYY secretory responses to valeric acid; that linoleic acid and conjugated linoleic acid 9,11 (CLA 9,11) are potent PYY secretagogues; and that chronic exposure of SCFAs and LCFAs can be detrimental to STC-1 cells. Our studies demonstrate the potential usefulness of STC-1 cells as an in vitro model for investigating nutrient-stimulated PYY secretion in an acute setting. Furthermore, our discovery that CLA directly stimulates L-cells to secrete PYY indicates another possible mechanism contributing to the observed effects of dietary CLA on weight loss.

Dietary supplementation of conjugated linoleic acid in horses increases plasma conjugated linoleic acid and decreases plasma arachidonic acid but does not alter body fat

Studies using dietary supplementation of eicosapentaenoic and docosahexaenoic fatty acids (FA) in horses report inconsistent anti-inflammatory results but consistently report an increase in plasma arachidonic acid (C20:4), the major substrate of cyclooxygenase (COX) II inflammatory pathway. Conjugated linoleic acid has shown anti-inflammatory effects in laboratory and food animal species, but effects of CLA supplementation in horses have not been reported. Our objective was to determine the effects of CLA supplementation on plasma CLA and C20:4 and body fat in healthy horses at maintenance. In a crossover study, 12 mature mares were blocked by breed, age, and BCS and separated into 2 treatment groups (n = 6/group). Groups were fed CLA and corn oil (CO; isocaloric control) for two 6-wk feeding periods, separated by a 4-wk period during which treatment was withheld. Corn oil or CLA supplement (55% mixed CLA isomers) was incorporated into diets at 0.01% BW/d. Mares were fed individually and restricted to dry lots to control forage intake. Rump fat thickness (RFT), BW, and BCS were measured before (d 0) and after (d 42) each feeding period. Blood was collected on d 0, 14, 28, and 42 of each 6-wk period for GLC analysis of plasma CLA isomers (cis-9, trans-11; trans-10, cis-12; and trans-9, trans-11) and C20:4. An ANOVA was conducted to compare the response of RFT, BW, and BCS of CLA-treated and control mares. A mixed methods analysis with repeated measures was used to detect differences in plasma FA concentrations. There were no differences in BW, RFT, or BCS between treatment groups. All CLA isomers present in the CLA supplement were greater in plasma of horses fed CLA compared with controls (P < 0.01). Additionally, plasma concentrations of C20:4 were decreased in horses fed CLA (P < 0.05). This decline in C20:4 may impact the COX II pathway and warrants further investigation. These results suggest that in an equine model, dietary CLA increases circulating concentrations of supplemented CLA isomers and decreases circulating C20:4. Examining physiological effects of CLA supplementation in horses at varying levels of growth, exercise, and progression of joint disease may offer insight to potential benefits of CLA in the horse.

CLA prevents alterations in glycolytic metabolites induced by a high fat diet

CLA has been reported to have beneficial and controversial effects on glucose and lipid metabolism. Besides, high fat (HF) diets induce alterations in liver and muscle lipid deposition, which could be associated with anomalous glucose utilization. Therefore, our aim was to evaluate whether the intake of CLA could prevent alterations in glycolytic intermediate metabolites and glycogen deposition induced by a HF diet. For this purpose, growing mice were fed a control diet (7% corn oil), a HF diet (20% corn oil), or a HF diet containing 17% corn oil + 3% CLA for 30 days. Liver and muscle glucose intermediate metabolites and glycogen were assessed. Liver glycolysis was inhibited by HF, reflected by a decreased flow of substrates through phosphofructokinase-1α linked to elevated citrate. CLA at HF diet prevented these alterations while increasing the lactate and glycogen synthesis. In the muscle, the HF diet emphasized the reduction of the flux through phosphofructokinase-1α, without additional changes in total glycogen levels. In conclusion, dietary CLA partially prevented glycolytic pathway alterations in the liver but not in the muscle of mice fed a HF diet, associated with adverse effects as sustained hyperglycemia and hepatic lactate accumulation. Practical applications: The present study evaluates the potential use of CLA and its consequences on several aspects of glucose metabolism. Considering that the FDA has recently approved CLA as a Generally Recognized as Safe (GRAS) category, a measure that will foster the commercial production of food and beverages with CLA supplementation, we believe it is relevant to study its potential functional properties on glucose metabolism in an experimental animal model characterized by alterations in liver and muscle lipid deposition.

Effect of CLA on performance and immune response of weanling piglets1

An experiment was conducted to evaluate the effect of CLA on the immune response and performance of piglets when subjected to an immune challenge. A total of 32 weanling pigs (17 to 23 d of age) with an initial BW of 8.9 kg were allotted to a 3 × 2 factorial arrangement of treatments. There were 3 levels of dietary CLA (0%, 1%, and 2%) and 2 levels of lipopolysaccharide (LPS) challenge (unchallenged and challenged). Challenged pigs were challenged on d 7 and 21. On d 4 and 18, all pigs were inoculated with BSA for assessment of IgG production. There was no difference in growth performance among piglets receiving different CLA supplementation levels. However, LPS-challenged piglets had poorer BW (P < 0.05), ADFI (P < 0.01), and ADG (P < 0.001) compared with the control group at d 35 postweaning. Lipopolysaccharide-challenged piglets also had increased respiratory rate (P < 0.001) and rectal temperature (P < 0.001), and decreased plasma proteins, hematocrit, and white blood cell counts (P < 0.05). Production of IgG against BSA was increased in the 1% CLA supplementation group (P < 0.001), indicating that CLA has an immunomodulatory effect. Supplementation with CLA did not affect lymphocyte proliferation, percentage of CD4(+) and CD8(+) cells, plasma proteins, red and white blood cell count, respiratory rate, or rectal temperature after LPS challenge. Although CLA supplementation did not influence growth performance or certain immune system measurements, the increased IgG titers with 1% CLA dietary supplementation indicate that it has a beneficial effect on the humoral immune system of weaned piglets.

Hepatic Metabolic, Inflammatory, and Stress-Related Gene Expression in Growing Mice Consuming a Low Dose ofTrans-10,cis-12-Conjugated Linoleic Acid

Dietary trans-10, cis-12-conjugated linoleic acid (trans-10, cis-12-CLA) fed to obese and nonobese rodents reduces body fat but leads to greater liver mass due to steatosis. The molecular mechanisms accompanying such responses remain largely unknown. Our study investigated the effects of chronic low trans-10, cis-12-CLA supplementation on hepatic expression of 39 genes related to metabolism, inflammation, and stress in growing mice. Feeding a diet supplemented with 0.3% trans-10, cis-12-CLA (wt/wt basis) for 6 weeks increased liver mass and concentration of long-chain fatty acids (LCFAs) in liver, while adipose tissue mass decreased markedly. These changes were accompanied by greater expression of genes involved in LCFA uptake (Cd36), lipogenesis, and triacylglycerol synthesis (Acaca, Gpam, Scd, Pck1, Plin2). Expression of these genes was in line with upregulation of the lipogenic transcription factor Srebf1. Unlike previous studies where higher >0.50% of the diet) doses of trans-10, cis-12-CLA were fed, we found greater expression of genes associated with VLDL assembly/secretion (Mttp, Cideb), ketogenesis (Hmgcs2, Bdh1), and LCFA oxidation (Acox1, Pdk4) in response to trans-10, cis-12-CLA. Dietary CLA, however, did not affect inflammation- and stress-related genes. Results suggested that a chronic low dose of dietary CLA increases liver mass and lipid accumulation due to activation of lipogenesis and insufficient induction of LCFA oxidation and VLDL assembly/secretion.

Effects of conjugated linoleic acid on oxidative stress in rats with sucrose-induced non-alcoholic fatty liver disease

The effect of CLA on hepatic oxidative stress and its relationship with the non-alcoholic fatty liver disease in rats was evaluated. Twenty-one days old Wistar rats were divided in two groups: the control group of six rats, which received a standard diet; and the sucrose group of 12 rats, which was given the same standard diet plus 30% sucrose in the drinking water. After 9weeks the animals of the sucrose group were divided in two sub-groups of six rats each: the vegetable oil group that was fed 7.5% sunflower oil in the diet, and the CLA group which received 1.5% CLA. After 8weeks the animals were sacrificed to obtain blood and liver tissue samples. Levels of oxidative stress markers: SOD, GSH, and catalase were measured in serum and liver homogenate and histological analysis was performed to recognize steatosis. Dietary CLA significantly decreased body fat, glutathione peroxidase, and superoxide dismutase in serum and liver. The histological analysis showed that, although CLA consumption was clearly beneficial, it did not entirely prevent sucrose-induced steatosis.