[Fatty acid patterns of rat liver during feeding of even- or odd-numbered medium chain triglycerides and varying amounts of linoleic acid].
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Animals↗
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Results for “LINOLEIC ACID”
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Incorporation of linoleic acid by the cestode Hymenolepis diminuta (Rudolphi, 1819).
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Animals↗
Does low dietary intake of linoleic acid predispose to myocardial infarction?
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Dietary Fats↗
Dietary and adipose tissue content of linoleic acid in 40-year old men.
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Adipose Tissue↗
Inhibitory effect of conjugated dienoic derivatives of linoleic acid and beta-carotene on the in vitro growth of human cancer cells.
The effects of physiologic concentrations of conjugated linoleic acid (CLA) and beta-carotene were assessed on human (M21-HPB, malignant melanoma; HT-29, colorectal; MCF-7, breast) cancer cells. The incubation of cancer cells with CLA showed significant reductions in proliferation (18-100%) compared to control cultures. M21-HPB and MCF-7 cell mortality was dose- and time-dependent. beta-Carotene was inhibitory to breast cells only. MCF-7 cells supplemented with CLA incorporated significantly less [3H]leucine (45%), [3H]uridine (63%) and [3H]thymidine (46%) than control cultures. M21-HPB and HT-29 cells supplemented with CLA incorporated less [3H]leucine (25-30%). These in vitro results suggest that CLA and beta-carotene may be cytotoxic to human cancer cells in vivo.
Breast Neoplasms↗
Conjugated linoleic acid--mediated apoptosis in Jurkat T cells involves the production of reactive oxygen species.
The pro-apoptotic ability of conjugated linoleic acid (CLA) has been partly accounted for its anticarcinogenic effect although the precise mechanism of action remains elusive. In this study we characterized the biochemical events governing CLA-mediated apoptosis in Jurkat T cells. CLA induced a time-and dose-dependent activation of caspase-3. Pre-treatment with antioxidant molecules (trolox and quercetin), antioxidant enzymes (catalase and superoxide dismutase) metal chelator (EDTA), reducing agent (N-acetyl-L-cysteine), NADPH oxidase or protein kinase C (PKC) inhibitor (diphenyleneiodinium and G 6976, respectively) suppressed CLA-mediated caspase-3 activation. Moreover, CLA treatment increased the NADPH oxidase activity and depleted the intracellular pool of reduced glutathione. These results suggested that CLA can trigger apoptosis through an oxidative stress mediated by the PKC/NADPH oxidase pathway. The proposed mechanism provides a new insight into the anticancer activity of CLA.
Apoptosis↗
Conjugated linoleic acid reduces body fat in healthy exercising humans.
This study was designed to investigate the efficacy and tolerability of daily conjugated linoleic acid (CLA) in healthy exercising humans. This was a random-double-blind, placebo-controlled study in 20 healthy humans of normal body weight and body mass index less than 25.0 kg/m2, who did standardized physical exercise in a gym for 90 min three times weekly. Participants took either placebo (hydrogel) or CLA 0.6 g [DOSAGE ERROR CORRECTED], three times daily, as two capsules during meals, for 12 weeks. Body fat, measured using near infrared light, was significantly reduced in the CLA group during the study, but not in the placebo group. No effects on body weight were observed. Tolerability was good and similar in the two groups. Compliance, as judged by the number of returned capsules, was more than 80% of the recommended dose for all participants. Thus CLA reduces body fat but not body weight in healthy exercising humans of normal body weight.
Adipose Tissue↗
[Effect of conjugated linoleic acid on PPAR gamma gene expression and serum leptin in obese rat].
OBJECTIVE: In order to study the effect of conjugated linoleic acid on PPAR gamma gene expression, serum leptin, blood glucose and blood lipid level. METHODS: Five groups of male Wistar rats were randomly selected and fed with different diets (basic diet, high-fat diet, high-fat with 0.75% CLA, high-fat with 1.50% CLA, and high-fat with 3.00% CLA) for 12 weeks. At the end of experiment, the rats were sacrificed, the ratio of lipids to body weight were calculated, and the blood glucose, serum lipids, serum leptin were measured. RT-PCR was used for measuring the expression of PPAR gamma mRNA in white adipose tissue of rats. RESULTS: It was shown that the supplement of CLA could decrease decreased blood glucose, serum triglyceride, cholesterol and leptin levels, and increased the expression of PPAR gamma in white adipose tissue of obese rat. CONCLUSION: CLA could decrease blood glucose, serum lipids, and decrease the levels of leptin possibly via activating peroxisome proliferator--activated receptor gamma (PPAR gamma), resulting in the improvement of leptin resistance of obese rat.
Adipose Tissue↗
Effects of combination dietary conjugated linoleic acid with vitamin A (retinol) and selenium on the response of the immunoglobulin production in mice.
The dietary effect of conjugated linoleic acid (CLA) on the response of the immunoglobulin (serum and tissue) production in Balb/C mice was examined at three doses: 0 %(control), 0.5% and 1.5%. The combination effects of CLA with vitamin ADE or selenium also were investigated. CLA at 0.5% increased serum immunoglobulin A, G, mesenteric lymph node (MHN) and gut luminal IgA (secretory IgA) levels. However, 1.5% CLA decreased SIgG slightly. CLA both alone and combined with vitamin ADE and selenium did not affect serum IgE. The levels of immunoglobulin concentration in the 0.5% CLA group were higher than those in the 1.5% CLA group. The level of serum IgG in 1.5% CLA combined with selenium was maintained at the same level as that of control. It is considered that over- doses of CLA (1.5%) even depressed the production of immunoglobulin but selenium and/or vitamin inhibited this activity to a certain extent. In this study, dietary CLA increased immunoglobulin production in a dose-dependent manner. Vitamin ADE and Selenium combined with CLA also increased the immunoglobulin production response except serum IgE.
Animals↗
[Effects of c9, t11-conjugated linoleic acid on the metastasis of human gastric carcinoma cell line].
In order to study the effects of c9, t11-conjugated linoleic acid on the invasion of human gastric carcinoma cell line(SGC-7901) and explore its possible mechanism, the five levels of CLA in medium were designed as 0, 25, 50, 100 and 200 mmol/L respectively. After SGC-7901 were treated with c9, t11-CLA for 24 hours, the reconstituted basement membrane invasion assay was used to evaluate invasive ability of cancer cells. The type IV collagenase was assessed by PAGE substrate zymography and the expression of TIMP-1 and TIMP-2 mRNA was measured by RT-PCR. The result displayed that c9, t11-CLA could inhibit the reconstituted basement memebrane invasion, reduce type IV collagenase activities in the serum-free supernatant of SGC-7901 cells and induce TIMP-1 and TIMP-2 mRNA expression in SGC-7901 cell line. Therefore, it is suggested that CLA could inhibit the reconstituted basement membrane invasion of SGC-7901 cells and the anti-invasion action of c9, t11-CLA might be associated with the reduction of type IV collagenase activity in tumor cell culture supernatant and induction of tumor cell TIMP-1 and TIMP-2 mRNA expression.
Adenocarcinoma↗
Conjugated linoleic acid supplementation for 1 y reduces body fat mass in healthy overweight humans.
BACKGROUND: Short-term trials showed that conjugated linoleic acid (CLA) may reduce body fat mass (BFM) and increase lean body mass (LBM), but the long-term effect of CLA was not examined. OBJECTIVE: The objective of the study was to ascertain the 1-y effect of CLA on body composition and safety in healthy overweight adults consuming an ad libitum diet. DESIGN: Male and female volunteers (n = 180) with body mass indexes (in kg/m(2)) of 25-30 were included in a double-blind, placebo-controlled study. Subjects were randomly assigned to 3 groups: CLA-free fatty acid (FFA), CLA-triacylglycerol, or placebo (olive oil). Change in BFM, as measured by dual-energy X-ray absorptiometry, was the primary outcome. Secondary outcomes included the effects of CLA on LBM, adverse events, and safety variables. RESULTS: Mean (+/- SD) BFM in the CLA-triacylglycerol and CLA-FFA groups was 8.7 +/- 9.1% and 6.9 +/- 9.1%, respectively, lower than that in the placebo group (P < 0.001). Subjects receiving CLA-FFA had 1.8 +/- 4.3% greater LBM than did subjects receiving placebo (P = 0.002). These changes were not associated with diet or exercise. LDL increased in the CLA-FFA group (P = 0.008), HDL decreased in the CLA-triacylglycerol group (P = 0.003), and lipoprotein(a) increased in both CLA groups (P < 0.001) compared with month 0. Fasting blood glucose concentrations remained unchanged in all 3 groups. Glycated hemoglobin rose in all groups from month 0 concentrations, but there was no significant difference between groups. Adverse events did not differ significantly between groups. CONCLUSION: Long-term supplementation with CLA-FFA or CLA-triacylglycerol reduces BFM in healthy overweight adults.
Absorptiometry, Photon↗
Dietary conjugated linoleic acid lowers plasma cholesterol during cholesterol supplementation, but accentuates the atherogenic lipid profile during the acute phase response in hamsters.
Conjugated linoleic acid (CLA) reportedly exerts anticarcinogenic and antiatherosclerotic effects in animals. To test the hypothesis that the putative antiatherosclerotic effect of CLA might derive from an anti-inflammatory or antioxidant action on lipoprotein metabolism, an acute phase response (APR) was elicited in hamsters while varying dietary cholesterol and vitamin E intakes in two experiments. The effect of CLA intake (to 1%) was examined with 0% (Experiment 1, 7 wk) and 0 or 0.3% (Experiment 2, 12 wk) cholesterol, at which point APR was induced. In hamsters not fed dietary cholesterol (Experiment 1), CLA exaggerated the rise in plasma and LDL cholesterol observed during the APR. When CLA was fed concurrently with cholesterol (Experiment 2), plasma and liver cholesterol were reduced up to 40% independent of the APR. In addition, CLA decreased body weight gain and adipose reserves in Experiment 1, but not in Experiment 2. Because CLA failed to attenuate APR and was not influenced by vitamin E status, an antioxidant/anti-inflammatory role was not apparent. However, the reduced burden on liver and lipoprotein cholesterol induced by CLA during cholesterol feeding, suggests that CLA curtailed cholesterol absorption, whereas the rise during APR suggests that CLA exaggerated the impaired clearance of plasma cholesterol associated with acute inflammation.
Acute-Phase Reaction↗
[Effect of conjugated linoleic acid on gene expression of adiponectin of obese rat fed with high fat diet].
OBJECTIVE: To study the effect of conjugated linoleic acid (CLA) on expression of adiponectin in white adipose tissue of obese rats. METHODS: Male Wistar rats were randomly divided into control group, high-fat group and high fat + CLA group (0.75 g, 1.50 g, 3.00 g per hundred gram diet weight), we observed the effect of CLA on serum insulin and glucose levels of obese rats, and the reverse transcription polymerase chain reaction (RT-PCR) technique was used to measure the expression level of adiponectin and peroxisome proliferator-activated receptor-gamma (PPARgamma) mRNA. RESULTS: The serum insulin and glucose levels of obese rats were (11.11 +/- 2.73) microIU/ml, (5.09 +/- 0.66) mmol/L. The supplement of CLA decreased the hyperinsulinemia and hyperglycemia, the serum insulin in CLA group (0.75 g, 1.50 g, 3.00 g per hundred gram diet weight) were (6.99 +/- 1.77) microIU/ml, (7.36 +/- 1.48) microIU/ml, (7.85 +/- 1.60) microIU/ml (P < 0.05), and glucose were (4.28 +/- 0.72) mmol/L, (4.18 +/- 0.55) mmol/L (P < 0.05), (4.06 +/- 0.63) mmol/L (P < 0.05), CLA can increase the expression of adiponectin and PPARgamma in adipose tissue of obese rat. CONCLUSION: The CLA might improve the insulin resistance of the obese rat and increase the expression of adiponectin mRNA, which might possibly act through activating PPARgamma.
Adiponectin↗
[The effects of conjugated linoleic acid on the ability of murine macrophage in killing tumor cells].
OBJECTIVE: To study the effects of c9,t11-conjugated linoleic acid on the killing ability of macrophage to B16-MB cells in C57 mice and explore its possible mechanism. METHODS: The five levels of CLA was designed as 0, 25, 50, 75, 100 micro mol/L. After macrophage was treated with CLA for 24 h, the killing ability of macrophage on B16-MB cells was evaluated by MTT, The expression of C57 mice macrophage cytokine IL-6, TNF-alpha and iNOS mRNA was detected by RT-PCR. The expression of Erk protein was examined by Western Blot assay. RESULTS: The inhibitory effect of macrophage on tumor cell depend on the treatment of the increased c9,t11-CLA level, at the same time, the expression of IL-6, TNF-alpha and iNOS mRNA increased, the expression of Erk decreased with the elevating dose of CLA. CONCLUSIONS: c9,t11-CLA could increase the killing ability of macrophage in mice to B16-MB cells, and it was associated with induction of IL-6, TNF-alpha and iNOS mRNA expression. We speculate that antitumor ability of CLA may be associated with taking part in body immune regulation action, and the effects of CLA on the killing ability of murine macrophage to B16-MB cells was not associated with the MAPKErk pathway.
Animals↗
Effects of c9,t11-conjugated linoleic acid on adhesion of human gastric carcinoma cell line SGC-7901.
AIM: To investigate the effect of c9,t11-conjugated linoleic acid (c9,t11-CLA) on the adhesion of human gastric carcinoma cell line (SGC-7901). METHODS: SGC-7901 cells were at first treated with different concentrations (25, 50, 100, 200 micromol/L) of c9,t11-CLA and 1 mL/L ethanol (as a negative control) for 24 h. Using adhesion assay and Western blot, we investigated the ability of SGC-7901 cells to adhere to intracellular matrix and examined the expression of E-cadherin (ECD), alpha-catenin, intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) in these cells. RESULTS: The attachment rate to laminin of SGC-7901 cells treated with different concentrations of c9,t11-CLA (0, 25, 50, 100, and 200 micromol/L) was 100.0+/-3.3, 95.7+/-4.0, 89.2+/-4.6, 87.9+/-6.1, and 65.9+/-5.8, respectively. The attachment rate to fibronectin was 100.0+/-4.7, 96.8+/-3.8, 94.5+/-4.1, 76.5+/-4.3, and 61.8+/-4.8, respectively. The attachment rate to Matrigel was 99.9+/-6.6, 91.4+/-6.8, 85.5+/-7.4, 79.3+/-5.6, and 69.6+/-5.1, respectively. Besides, c9,t11-CLA could increase the level of ECD and alpha-catenin, and decrease the level of ICAM-1 and VCAM-1 in SGC-7901 cells. CONCLUSION: c9,t11-CLA can reduce the adhesion of human gastric carcinoma cells to laminin, fibronectin and Matrigel. c9,t11-CLA can increase the level of ECD and alpha-catenin, and decrease the level of ICAM-1 and VCAM-1 in human gastric carcinoma cells.
Animals↗
Effects of dietary conjugated linoleic acid supplementation on performance and immune function of weaned pigs.
Two experiments were conducted to evaluate the effect of dietary conjugated linoleic acid (CLA) on performance and immune responses of weaned pigs. In Exp. I, 72 crossbred pigs weaned at 19 to 23 days of age and weighing 7.20 +/- 0.11 kg were randomly allotted to four diets supplemented with CLA at 0, 1, 2 or 3%. On day 14, pigs were injected with ovalbumin (1mg per kg BW) and blood samples were collected on day 7 and 14 after injection to test the specific OVA antibody. In Exp. II, 36 crossbred pigs weaned at 26 to 30 days of age and weighing 8.12 +/- 0.14 kg were randomly divided into two diets containing either 0 or 2% CLA. On day 14 and 28, blood samples were obtained to determine the lymphocyte proliferation and PGE2 levels in both trials, and CD4+, CD8+ T cells subsets and interleukin-1beta production were tested in Exp. II. In Exp. I both average daily gain and average daily feed intake of weaned pigs were improved quadratically and feed efficiency was increased linearly by CLA supplementation. Lymphocyte proliferation response to concanavalin A was increased quadratically as dietary CLA concentration increased on day 14 and 28. Ovalbumin antibody production levels were increased linearly on day 7 after injection of ovalbumin and increased quadratically on day 14 after injection, which follows the increased CLA levels, whereas CLA reduced linearly the production of prostaglandin E2 (PGE2). The results of Exp. II indicated that CLA improved performance, lymphocyte proliferation, and increased the CD8+ lymphocyte population, while reduced the production of PGE2 and interleukin-lbeta (IL- 1beta). These results suggest that the supplementation of CLA enhanced lymphocyte proliferation function, possibly by regulating the PGE2 production, and improved growth performance of pigs. Further studies are needed to determine the mechanism of CLA-induced inhibition of IL-1beta production.
Animal Feed↗
Comparative toxicity of oleic and linoleic acid on human lymphocytes.
Commercially available lipid emulsions for parenteral nutrition are mainly composed by long chain triacylglycerol containing a high proportion of linoleic acid (LA) or oleic acid (OA). The immunological impact of such therapy is particularly important because parenteral diets are often administered to critically ill patients as a mechanism to supply adequate nutrition during catabolic stress conditions. The comparative toxicity of OA and LA on human lymphocytes and the type of cell death induced by these fatty acids were determined in vitro. Parameters of cell death were investigated by flow cytometry-cell viability, DNA fragmentation, phosphatidylserine externalization, mitochondrial depolarization, neutral lipid accumulation and production of reactive oxygen species-and by fluorescence microscopy-chromatin condensation. Additionally a spectrofluorometric assay was employed to determine the activities of caspase--3, 6 and 8. Evidence is presented herein that OA is less toxic to human lymphocytes than LA. However, both fatty acids promoted apoptosis and necrosis of these cells. The mechanism of cell death induced by OA involved activation of caspase 3 while the mechanism of death induced by LA involved mitochondrial depolarization and ROS production. Importantly, neutral lipid accumulation may be a mechanism to protect lymphocytes against the toxicity induced by OA. OA may offer an immunological less problematic alternative to LA with respect to fatty acid composition of parenteral nutritional emulsions.
Cell Survival↗
Effect of apoptosis on gastric adenocarcinoma cell line SGC-7901 induced by cis-9, trans-11-conjugated linoleic acid.
AIM: To determine the effect of apoptosis on gastric cancer cells (SGC-7901) induced by cis-9, trans-11-conjugated linoleic acid (c9, t11-CLA) and its possible mechanism in the inhibition of cancer cells growth. METHODS: Using cell culture, flow cytometery and immunocytochemical techniques, we examined the cell growth, frequency of apoptosis and distribution of cell cycle, expression of ki67, bcl-2, Fas, and c-myc of SGC-7901 cells which were treated with various c9, t11-CLA concentrations (25,50,100 and 200 micromol x L(-1)) of c9, t11-CLA for 24 h and 48 h, with a negative control (0.1 % ethanol). RESULTS: The growth of SGC-7901 cells was inhibited by c9,t11-CLA. Eight days after treatment with various concentrations of c9,t11-CLA, as mentioned above, the inhibition rates were 5.9 %, 20.2 %,75.6 % and 82.4 %, respectively. The frequency of apoptosis on SGC-7901 cells induced by different concentrations of c9, t11-CLA (except for 25 micromol.L(-1), 24 h) was significantly greater than that in the negative control (P<0.01). To further investigate the influence of the cell cycle progression, we found that apoptosis induced by c9, t11-CLA may be involved in blocking the cell cycle of SGC-7901 cells. Immunocytochemical staining demonstrated that SGC-7901 cells preincubated in media supplemented with different c9, t11-CLA concentrations for various time periods significantly decreased the expressions of ki67 (the expression rates were 18.70-3.20 %, at 24 h and 8.10-0.20 % at 48 h, respectively), bcl-2 (4.30-0.15 % at 24 h and 8.05 %-0 at 48 h), and c-myc (4.85-2.20 % at 24 h and 4.75-0.30 % at 48 h) as compared with those in the controls (the expressions of ki67, bcl-2, and c-myc were 15.1 % at 24 h and 13.5 % at 48 h, 6.80 % at 24 h and 8.00 % at 48 h, 5.50 % at 24 h and 5.30 % at 48 h, respectively) (P<0.01), whereas the expressions of Fas were increased (0.60-2.75 %, 24 h and 0.45-5.95 %, 48 h). CONCLUSION: The growth and proliferation of SGC-7901 cells are inhibited by c9, t11-CLA via blocking the cell cycle, pathways of bcl-2-associated mitochondria with reduced expression of bcl-2 and Fas-associated death domain protein (FADD) with enhanced expression of Fas. But expression of c-myc on SGC-7901 cells is lower than that in negative control, which needs to be studied further.
Adenocarcinoma↗