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Zeyuan Deng - One of the best experts on this subject based on the ideXlab platform.
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linolElaidic Acid induces apoptosis cell cycle arrest and inflammation stronger than Elaidic Acid in human umbilical vein endothelial cells through lipid rafts
European Journal of Lipid Science and Technology, 2017Co-Authors: Huan Rao, Qiu Bin, Yawei Fan, Zeyuan DengAbstract:Lipid rafts were reported to play important roles in Elaidic Acid-induced apoptosis in human umbilical vein endothelial cells (HUVECs). LinolElaidic Acid induced cell injury more seriously than Elaidic Acid. However, whether lipid rafts may play the same roles for linolElaidic Acid- and Elaidic Acid-induced cell injury was unknown. Therefore, the aim of this study was to compare the effect of lipid rafts on linolElaidic Acid- and Elaidic Acid-induced apoptosis, cell cycle arrest and inflammation in HUVECs. The cell viability was significantly decreased, the number of apoptotic cells and cell population in G1 phase were significantly increased in Elaidic Acid- or linolElaidic Acid-treated cells, compared to methyl-β-cyclodextrin + trans-fatty Acids-treated cells. In addition, the expression levels of pro-apoptotic proteins (caspase-3, -8, Bax, p53) and inflammation factors (vascular cell adhesion molecule-1, intercellular adhesion molecule, E-selectin and nitro oxide) were significantly increased, and anti-apoptotic protein like Bcl-2 decreased significantly in linolElaidic Acid-treated cells, which were stronger than those in Elaidic Acid-treated cells. In conclusion, linolElaidic Acid induces a stronger lesion effect on HUVECs through lipid rafts compared to Elaidic Acid. Practical applications: Different processing method generated different trans fatty Acids, such as industrial hydrogenation produced amount of trans 18:1, deep frying with temperature over 200°C generated both trans 18:1 and trans 18:2. Researches reported that trans fatty Acids with different saturation had diverse effect on human health, especially cardiovascular disease. This paper found that 9t12t18:2 induced a stronger lesion effect on HUVECs compared with 9t18:1 through lipid rafts, which indicated that we should pay attention to 9t12t18:2 produced from deep frying, and the deep frying temperature should be dropped to reduce the trans 18:2 level. Moreover, the involvement of lipid rafts in trans fatty Acids induced apoptosis, cell cycle arrest and inflammation was demonstrated, which provided a scientific basis for the prevention and treatment of cardiovascular disease. Both linoElaidic Acid and Elaidic Acid induced HUVECs apoptosis and increased expression of pro-apoptotic proteins. However, supplementation of TFAs to MβCD-treated cells increased the cell viability and significantly decreased the number of apoptotic cells. Moreover, linolElaidic Acid induces a stronger lesion effect on HUVECs by lipid rafts mediation compared to Elaidic Acid.
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Potential Pathways Involved in Elaidic Acid Induced Atherosclerosis in Human Umbilical Vein Endothelial Cells
Hindawi Limited, 2017Co-Authors: Zhongshang Liang, Bin Qiu, Ting Luo, Zeyuan DengAbstract:Researches have demonstrated that trans-fatty Acids are related to the progression of atherosclerosis, but the underlying mechanism is not clear till now. In the presented study, two-dimensional electrophoresis based proteomics was used to discover the role of Elaidic Acid in atherosclerosis. In human umbilical vein endothelial cells (HUVEC), twenty-two and twenty-three differentially expressed proteins were identified in low (50 μmol/L) and high (400 μmol/L) concentration Elaidic Acid simulated groups, respectively, comparing with the control group. The expressions of some selected proteins (PSME3, XRCC5, GSTP1, and GSTO1) were validated by qRT-PCR analysis. Western blotting analysis further confirmed that Elaidic Acid downregulated the expression of PSME3 and XRCC5. Moreover, P53, the downstream protein of PSME3, was further investigated. Results demonstrated that a variety of proteins, many of which were related to oxidative stress, apoptosis, and DNA damage, were involved in the Elaidic Acid induced atherosclerosis. Furthermore, P53 was demonstrated to regulate the atherosclerosis through cell cycle arrest and apoptosis pathway
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lipid rafts and fas fasl pathway may involve in Elaidic Acid induced apoptosis of human umbilical vein endothelial cells
Journal of Agricultural and Food Chemistry, 2014Co-Authors: Huan Rao, Zeyuan Deng, Yawei FanAbstract:Our previous study showed that trans-fatty Acids can cause apoptosis of endothelial cells through the caspase pathway and the mitochondrial pathway. The objective of this study was to explore how trans-fatty Acids activate the caspase pathway, whether there exist specific receptors induced apoptosis by comparing normal cells and non-rafts cells treated with Elaidic Acid (9t18:1) and oleic Acid (9c18:1), respectively. Compared to normal cells treated with 9t18:1, the cell viability increased by 13% and the number of apoptotic cells decreased by 3% in non-rafts cells treated with 9t18:1 (p < 0.05), and the expression levels of pro-apoptotic proteins such as caspase-3, -8, -9, Bax, and Bid decreased, and expression of antiapoptotic protein Bcl-2 increased (p < 0.05). In addition, Fas/FasL expression in cell membrane decreased significantly (p < 0.05). In conclusion, the lipid rafts and Fas/FasL pathway may involve in 9t18:1-induced apoptosis of human umbilical vein endothelial cells.
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linolElaidic Acid induces a stronger proliferative effect on human umbilical vein smooth muscle cells compared to Elaidic Acid
Lipids, 2013Co-Authors: Ting Luo, Yawei Fan, Rong Liu, Xiaoru Liu, Zeyuan DengAbstract:Trans fatty Acids (TFA) have been considered as an independent risk factor of coronary heart disease, sudden death and insulin-resistance, and different TFA isomers may have different effects on the progression of cardiovascular diseases such as atherosclerosis. The aim of the study was to investigate the effects of two major TFA, Elaidic Acid and linolElaidic Acid which have the same number of carbons but a different number and configuration of trans bonds, on the proliferation of human umbilical vein smooth muscle cells (HUVSMC). Methyl thiazolyl tetrazolium and flow cytometry assays showed that the cell proliferation rose to 115.37 ± 0.39 and 117.5 ± 0.57 % and the cell number in the S phase of the cell cycle reached 27.7 ± 0.7 and 25.8 ± 2.8 % when treated with 50 μM Elaidic Acid and 20 μM linolElaidic Acid, respectively. Quantitative real-time reverse transcriptase-polymerase chain reaction and Western blotting analyses showed that the two TFA increased the mRNA and protein expression levels of PCNA, CDK2 and Cyclin E in HUVSMC. Moreover, gas chromatography analysis showed that the total PUFA level of HUVSMC was lower after treatment with the two TFA, especially n-3 PUFA. These results suggested that linolElaidic Acid exhibited a stronger proliferative effect on HUVSMC than Elaidic Acid, and regulation of CDK2 and Cyclin E may be important for the effect of the TFA on atherosclerosis.
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caspase pathway of Elaidic Acid 9t c18 1 induced apoptosis in human umbilical vein endothelial cells
Cell Biology International, 2012Co-Authors: Bin Qiu, Yawei Fan, Rong Liu, Zeyuan DengAbstract:Although TFAs (trans fatty Acids) do have effects on many endothelial functions, systemic inflammation and immune disorders, only limited experimental evidence is available that TFAs participate in the pathogenesis of endothelial cell apoptosis. HUVEC (human umbilical vein endothelial cells) were grown in medium with Elaidic Acid (9t-C18:1) at 50, 100, 200 and 400 μmol/l for 24 h. Apoptosis was measured by flow cytometry, and caspase 3, 8 and 9 activities by colorimetric assay and their mRNA expression by qRT-PCR (quantitative real-time PCR). Results showed that 9t-C18:1 induced apoptosis of HUVEC in a dose-dependent manner. The activities and mRNA expression of caspases 8, 9 and 3 were significantly increased compared with that of the control. Z-IETD-FMK and Z-LEHD-FMK inhibited the activation of caspase 3 and apoptosis induced by 9t-C18:1. Also Z-IETD-FMK inhibited the activation of caspase 9. mRNA expressions of Bid and Smac (second mitochondria-derived activator of caspase)/DIABLO [direct IAP (inhibitor of apoptosis)-binding protein with low pI] were also significantly elevated. We conclude that 9t-C18:1 induces apoptosis of HUVEC through activating caspases 8, 9 and 3. The death receptor pathway and the mitochondrial pathway both participated in the apoptosis course induced by 9t-C18:1.
Yawei Fan - One of the best experts on this subject based on the ideXlab platform.
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linolElaidic Acid induces apoptosis cell cycle arrest and inflammation stronger than Elaidic Acid in human umbilical vein endothelial cells through lipid rafts
European Journal of Lipid Science and Technology, 2017Co-Authors: Huan Rao, Qiu Bin, Yawei Fan, Zeyuan DengAbstract:Lipid rafts were reported to play important roles in Elaidic Acid-induced apoptosis in human umbilical vein endothelial cells (HUVECs). LinolElaidic Acid induced cell injury more seriously than Elaidic Acid. However, whether lipid rafts may play the same roles for linolElaidic Acid- and Elaidic Acid-induced cell injury was unknown. Therefore, the aim of this study was to compare the effect of lipid rafts on linolElaidic Acid- and Elaidic Acid-induced apoptosis, cell cycle arrest and inflammation in HUVECs. The cell viability was significantly decreased, the number of apoptotic cells and cell population in G1 phase were significantly increased in Elaidic Acid- or linolElaidic Acid-treated cells, compared to methyl-β-cyclodextrin + trans-fatty Acids-treated cells. In addition, the expression levels of pro-apoptotic proteins (caspase-3, -8, Bax, p53) and inflammation factors (vascular cell adhesion molecule-1, intercellular adhesion molecule, E-selectin and nitro oxide) were significantly increased, and anti-apoptotic protein like Bcl-2 decreased significantly in linolElaidic Acid-treated cells, which were stronger than those in Elaidic Acid-treated cells. In conclusion, linolElaidic Acid induces a stronger lesion effect on HUVECs through lipid rafts compared to Elaidic Acid. Practical applications: Different processing method generated different trans fatty Acids, such as industrial hydrogenation produced amount of trans 18:1, deep frying with temperature over 200°C generated both trans 18:1 and trans 18:2. Researches reported that trans fatty Acids with different saturation had diverse effect on human health, especially cardiovascular disease. This paper found that 9t12t18:2 induced a stronger lesion effect on HUVECs compared with 9t18:1 through lipid rafts, which indicated that we should pay attention to 9t12t18:2 produced from deep frying, and the deep frying temperature should be dropped to reduce the trans 18:2 level. Moreover, the involvement of lipid rafts in trans fatty Acids induced apoptosis, cell cycle arrest and inflammation was demonstrated, which provided a scientific basis for the prevention and treatment of cardiovascular disease. Both linoElaidic Acid and Elaidic Acid induced HUVECs apoptosis and increased expression of pro-apoptotic proteins. However, supplementation of TFAs to MβCD-treated cells increased the cell viability and significantly decreased the number of apoptotic cells. Moreover, linolElaidic Acid induces a stronger lesion effect on HUVECs by lipid rafts mediation compared to Elaidic Acid.
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lipid rafts and fas fasl pathway may involve in Elaidic Acid induced apoptosis of human umbilical vein endothelial cells
Journal of Agricultural and Food Chemistry, 2014Co-Authors: Huan Rao, Zeyuan Deng, Yawei FanAbstract:Our previous study showed that trans-fatty Acids can cause apoptosis of endothelial cells through the caspase pathway and the mitochondrial pathway. The objective of this study was to explore how trans-fatty Acids activate the caspase pathway, whether there exist specific receptors induced apoptosis by comparing normal cells and non-rafts cells treated with Elaidic Acid (9t18:1) and oleic Acid (9c18:1), respectively. Compared to normal cells treated with 9t18:1, the cell viability increased by 13% and the number of apoptotic cells decreased by 3% in non-rafts cells treated with 9t18:1 (p < 0.05), and the expression levels of pro-apoptotic proteins such as caspase-3, -8, -9, Bax, and Bid decreased, and expression of antiapoptotic protein Bcl-2 increased (p < 0.05). In addition, Fas/FasL expression in cell membrane decreased significantly (p < 0.05). In conclusion, the lipid rafts and Fas/FasL pathway may involve in 9t18:1-induced apoptosis of human umbilical vein endothelial cells.
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linolElaidic Acid induces a stronger proliferative effect on human umbilical vein smooth muscle cells compared to Elaidic Acid
Lipids, 2013Co-Authors: Ting Luo, Yawei Fan, Rong Liu, Xiaoru Liu, Zeyuan DengAbstract:Trans fatty Acids (TFA) have been considered as an independent risk factor of coronary heart disease, sudden death and insulin-resistance, and different TFA isomers may have different effects on the progression of cardiovascular diseases such as atherosclerosis. The aim of the study was to investigate the effects of two major TFA, Elaidic Acid and linolElaidic Acid which have the same number of carbons but a different number and configuration of trans bonds, on the proliferation of human umbilical vein smooth muscle cells (HUVSMC). Methyl thiazolyl tetrazolium and flow cytometry assays showed that the cell proliferation rose to 115.37 ± 0.39 and 117.5 ± 0.57 % and the cell number in the S phase of the cell cycle reached 27.7 ± 0.7 and 25.8 ± 2.8 % when treated with 50 μM Elaidic Acid and 20 μM linolElaidic Acid, respectively. Quantitative real-time reverse transcriptase-polymerase chain reaction and Western blotting analyses showed that the two TFA increased the mRNA and protein expression levels of PCNA, CDK2 and Cyclin E in HUVSMC. Moreover, gas chromatography analysis showed that the total PUFA level of HUVSMC was lower after treatment with the two TFA, especially n-3 PUFA. These results suggested that linolElaidic Acid exhibited a stronger proliferative effect on HUVSMC than Elaidic Acid, and regulation of CDK2 and Cyclin E may be important for the effect of the TFA on atherosclerosis.
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caspase pathway of Elaidic Acid 9t c18 1 induced apoptosis in human umbilical vein endothelial cells
Cell Biology International, 2012Co-Authors: Bin Qiu, Yawei Fan, Rong Liu, Zeyuan DengAbstract:Although TFAs (trans fatty Acids) do have effects on many endothelial functions, systemic inflammation and immune disorders, only limited experimental evidence is available that TFAs participate in the pathogenesis of endothelial cell apoptosis. HUVEC (human umbilical vein endothelial cells) were grown in medium with Elaidic Acid (9t-C18:1) at 50, 100, 200 and 400 μmol/l for 24 h. Apoptosis was measured by flow cytometry, and caspase 3, 8 and 9 activities by colorimetric assay and their mRNA expression by qRT-PCR (quantitative real-time PCR). Results showed that 9t-C18:1 induced apoptosis of HUVEC in a dose-dependent manner. The activities and mRNA expression of caspases 8, 9 and 3 were significantly increased compared with that of the control. Z-IETD-FMK and Z-LEHD-FMK inhibited the activation of caspase 3 and apoptosis induced by 9t-C18:1. Also Z-IETD-FMK inhibited the activation of caspase 9. mRNA expressions of Bid and Smac (second mitochondria-derived activator of caspase)/DIABLO [direct IAP (inhibitor of apoptosis)-binding protein with low pI] were also significantly elevated. We conclude that 9t-C18:1 induces apoptosis of HUVEC through activating caspases 8, 9 and 3. The death receptor pathway and the mitochondrial pathway both participated in the apoptosis course induced by 9t-C18:1.
Jan J Enghild - One of the best experts on this subject based on the ideXlab platform.
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hepatocytes respond differently to major dietary trans fatty Acid isomers Elaidic Acid and trans vaccenic Acid
Proteome Science, 2015Co-Authors: Toke P Krogager, Lone Nielsen, Derya Kahveci, Thomas F Dyrlund, Carsten Scavenius, Kristian W Sanggaard, Jan J EnghildAbstract:It has been discussed if the adverse health effect associated with the ingestion of trans fatty Acids correlates with the food source, as the composition of the isomers varies in different foods. We have investigated the hepatocellular responses to the predominant trans fatty Acid isomers in industrially produced partially hydrogenated vegetable oils (Elaidic Acid) and products of ruminant origin (trans-vaccenic Acid). The responses of HepG2-SF cells exposed to 100 μM fatty Acids during 7 days were examined. Elaidic Acid decreased the cellular proliferation rate while trans-vaccenic Acid had no effect. Analysis of cellular triacylglycerol fractions showed, that both trans fatty Acids were metabolized by HepG2-SF cells, although Elaidic Acid, to a higher degree than trans-vaccenic, accumulated in the triacylglycerol fraction. Proteome analysis revealed that the overlap of differentially regulated proteins only contained four proteins, suggesting that the two trans fatty Acid isomers affect the cells in different ways. The data are available via ProteomeXchange with identifier PXD000760. Our investigations revealed that the hepatocellular response to the two most abundant dietary positional C18:1 trans fatty Acid isomers differ substantially. In addition, the results suggest that trans-vaccenic Acid does not affect cholesterol metabolism adversely compared to Elaidic Acid.
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effects of Elaidic Acid on lipid metabolism in hepg2 cells investigated by an integrated approach of lipidomics transcriptomics and proteomics
PLOS ONE, 2013Co-Authors: Lone Nielsen, Toke P Krogager, Clifford Young, Carla Ferreri, Ole Norregaard Jensen, Chryssostomos Chatgilialoglu, Jan J EnghildAbstract:Trans fatty Acid consumption in the human diet can cause adverse health effects, such as cardiovascular disease, which is associated with higher total cholesterol, a higher low density lipoprotein-cholesterol level and a decreased high density lipoprotein-cholesterol level. The aim of the study was to elucidate the hepatic response to the most abundant trans fatty Acid in the human diet, Elaidic Acid, to help explain clinical findings on the relationship between trans fatty Acids and cardiovascular disease. The human HepG2 cell line was used as a model to investigate the hepatic response to Elaidic Acid in a combined proteomic, transcriptomic and lipidomic approach. We found many of the proteins responsible for cholesterol synthesis up-regulated together with several proteins involved in the esterification and hepatic import/export of cholesterol. Furthermore, a profound remodeling of the cellular membrane occurred at the phospholipid level. Our findings contribute to the explanation on how trans fatty Acids from the diet can cause modifications in plasma cholesterol levels by inducing abundance changes in several hepatic proteins and the hepatic membrane composition.
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identification of a potential biomarker panel for the intake of the common dietary trans fat Elaidic Acid trans 9 c18 1
Journal of Proteomics, 2012Co-Authors: Toke P Krogager, Lone Nielsen, Steffen Bak, Clifford Young, Carla Ferreri, Ole Norregaard Jensen, Peter Hojrup, Vladimiros Thoma, Ida B Thogersen, Jan J EnghildAbstract:Trans fatty Acid intake has been correlated to an unfavorable plasma lipoprotein profile and an increased cardiovascular disease risk. The present study aimed to identify a plasma protein biomarker panel related to human intake of Elaidic Acid. The human liver cell line HepG2-SF was used as a model system, and the cells were maintained for seven days in serum-free medium containing 100 μM Elaidic Acid (trans∆9-C18:1), oleic Acid (cis∆9-C18:1) or stearic Acid (C18:0). The secretomes were analyzed by stable isotope labeling of amino Acids in cell culture (SILAC), difference in gel electrophoresis (DIGE) and gene expression microarray analysis. Twelve proteins were found to be differentially regulated based on SILAC data (>1.3 fold change, P-value 1.3 fold change, P-value 1.3 fold change, P-value<0.01) following the addition of Elaidic Acid compared to oleic Acid or stearic Acid. The results revealed that 37 proteins were regulated specifically in response to Elaidic Acid exposure, and nine of these proteins were confirmed to be regulated in this manner by using selected reaction monitoring mass spectrometry.
Stéphane Guyot - One of the best experts on this subject based on the ideXlab platform.
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Comparison of the effects of major fatty Acids present in the Mediterranean diet (oleic Acid, docosahexaenoic Acid) and in hydrogenated oils (Elaidic Acid) on 7-ketocholesterol-induced oxiapoptophagy in microglial BV-2 cells
Chemistry and Physics of Lipids, 2017Co-Authors: Meryam Debbabi, Amira Zarrouk, Maryem Bezine, Wiem Meddeb, Thomas Nury, Asmaa Badreddine, El Mostafa Karym, Randa Sghaier, Lionel Brétillon, Stéphane GuyotAbstract:Increased levels of 7-ketocholesterol (7KC), which results mainly from cholesterol auto-oxidation, are often found in the plasma and/or cerebrospinal fluid of patients with neurodegenerative diseases and might contribute to activation of microglial cells involved in neurodegeneration. As major cellular dysfunctions are induced by 7KC, it is important to identify molecules able to impair its side effects. Since consumption of olive and argan oils, and fish is important in the Mediterranean diet, the aim of the study was to determine the ability of oleic Acid (OA), a major compound of olive and argan oil, and docosahexaenoic Acid (DHA) present in fatty fishes, such as sardines, to attenuate 7KC-induced cytotoxic effects. Since Elaidic Acid (EA), the trans isomer of OA, can be found in hydrogenated cooking oils and fried foods, its effects on 7KC-induced cytotoxicity were also determined. In murine microglial BV-2 cells, 7KC induces cell growth inhibition, mitochondrial dysfunctions, reactive oxygen species overproduction and lipid peroxidation, increased plasma membrane permeability and fluidity, nuclei condensation and/or fragmentation and caspase-3 activation, which are apoptotic characteristics, and an increased LC3-II/LC3-I ratio, which is a criterion of autophagy. 7KC is therefore a potent inducer of oxiapoptophagy (OXIdation + APOPTOsis + autoPHAGY) on BV-2 cells. OA and EA, but not DHA, also favor the accumulation of lipid droplets revealed with Masson's trichrome, Oil Red O, and Nile Red staining. The cytotoxicity of 7KC was strongly attenuated by OA and DHA. Protective effects were also observed with EA. However, 7KC-induced caspase-3 activation was less attenuated with EA. Different effects of OA and EA on autophagy were also observed. In addition, EA (but not OA) increased plasma membrane fluidity, and only OA (but not EA) was able to prevent the 7KC-induced increase in plasma membrane fluidity. Thus, in BV-2 microglial cells, the principal fatty Acids of the Mediterranean diet (OA, DHA) were able to attenuate the major toxic effects of 7KC, thus reinforcing the interest of natural compounds present in the Mediterranean diet to prevent the development of neurodegenerative diseases.
Paul J Nestel - One of the best experts on this subject based on the ideXlab platform.
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plasma cholesteryl ester transfer protein activity is increased when trans Elaidic Acid is substituted for cis oleic Acid in the diet
Atherosclerosis, 1994Co-Authors: Mavis Abbey, Paul J NestelAbstract:The trans isomer of oleic Acid (Elaidic Acid) increases low density lipoprotein (LDL) cholesterol and decreases high density lipoprotein (HDL) cholesterol in man. One possible mechanism for this effect is that trans fatty Acids increase plasma cholesteryl ester transfer protein (CETP) activity. We examined the effect of dietary trans fatty Acids on activity of this protein in plasma from 27 men in a double blind crossover comparison. The background diet, containing 15% energy as fat from dairy products, meat, bread and cereals, was supplemented with oleic or Elaidic Acid providing a further 20% energy. The Elaidic supplement provided about 6% energy as trans fatty Acid. Activity of CETP in plasma was significantly higher (P < 0.001) after the Elaidic Acid-rich diet (23.95 +/- 1.26%) compared with the diet enriched with oleic Acid (19.61 +/- 0.89%). A significant correlation between the change in plasma trans 18:1 fatty Acids and the change in plasma CETP activity (r = 0.58, P < 0.002) was independent of changes in LDL-cholesterol. The increase in CETP activity was in turn significantly correlated with a fall in HDL-cholesterol among subjects during the Elaidic Acid-rich period (r = -0.57, P < 0.01). We have shown that CETP demonstrates substrate specificity and that the increase in activity with dietary trans fatty Acids may contribute to a more atherogenic lipoprotein profile.
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plasma lipoprotein lipid and lp a changes with substitution of Elaidic Acid for oleic Acid in the diet
Journal of Lipid Research, 1992Co-Authors: Paul J Nestel, Manny Noakes, Bryan Belling, Rosemary Mcarthur, Peter M Clifton, E D Janus, Mavis AbbeyAbstract:The effect of additional dietary tmm fatty Acids (7% energy) on plasma lipids was assessed in a double-blind compar- ison of four separate diets: 1, enriched with butter fat (lauric- myristic-palmitic); 2, oleic Acid-rich; 3, Elaidic Acid-rich; 4, palmitic Acid-rich. The total dietary period was 11 weeks and comprised normal foods plus specific fat supplements. In 27 mildly hypercholesterolemic men, total and LDL cholesterol were significantly lower during the 3-week oleic Acid-rich diet, and were similar during the other three diets. For the four diets LDL cholesterol levels were in mg/dl: 1, 163; 2, 151; 3, 165; 4, 161. HDL cholesterol was significantly higher with the palmitic Acid-rich diet, 42 mg/dl, compared with Elaidic Acid, 38 mg/dl, which in turn was not lower than with oleic Acid, 38 mg/dl. Plasma Elaidic Acid concentration rose seven-fold with the tram fatty Acid diet but did not increase the vulnerability of LDL to oxidative change. The Elaidic Acid-rich diet led to significant ele- vations in the level of Lp(a) compared to all the other test diets. The Lp(a) level increased to 296 f 220 U/1 in the Elaidic Acid- rich period from 235 + 182 (mean + SD) in the first ("butter") period (P < 0.001) compared with 249 * 204 in the palmitic Acid period (E' < 0.001) and 236 + 201 in the oleic Acid period (NS). I We conclude that 3 weeks consumption of tram fatty Acid (mainly Elaidic) at about 7% energy (probably twice the Australian average) results in LDL cholesterol levels that do not differ from those seen with diets enriched with palmitic Acid or butter fat and are higher than when oleic Acid is substituted for Elaidic Acid.-Nestel, P., M. Noakes, B. Belling, R. McArthur, P. Clifton, E. Janus, and M. Abbey. Plasma lipoprotein lipid and Lp(a) changes with substitution of Elaidic Acid for oleic Acid in the diet. J. Lipid Res. 1992. 33: 1029-1036.
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plasma lipoprotein lipid and lp a changes with substitution of Elaidic Acid for oleic Acid in the diet
Journal of Lipid Research, 1992Co-Authors: Paul J Nestel, Manny Noakes, Bryan Belling, Rosemary Mcarthur, Peter M Clifton, Edward Janus, Mavis AbbeyAbstract:The effect of additional dietary trans fatty Acids (7% energy) on plasma lipids was assessed in a double-blind comparison of four separate diets: 1, enriched with butter fat (lauric-myristic-palmitic); 2, oleic Acid-rich; 3, Elaidic Acid-rich; 4, palmitic Acid-rich. The total dietary period was 11 weeks and comprised normal foods plus specific fat supplements. In 27 mildly hypercholesterolemic men, total and LDL cholesterol were significantly lower during the 3-week oleic Acid-rich diet, and were similar during the other three diets. For the four diets LDL cholesterol levels were in mg/dl: 1, 163; 2, 151; 3, 165; 4, 161. HDL cholesterol was significantly higher with the palmitic Acid-rich diet, 42 mg/dl, compared with Elaidic Acid, 38 mg/dl, which in turn was not lower than with oleic Acid, 38 mg/dl. Plasma Elaidic Acid concentration rose seven-fold with the trans fatty Acid diet but did not increase the vulnerability of LDL to oxidative change. The Elaidic Acid-rich diet led to significant elevations in the level of Lp[a] compared to all the other test diets. The Lp[a] level increased to 296 +/- 220 U/l in the Elaidic Acid-rich period from 235 +/- 182 (mean +/- SD) in the first ("butter") period (P less than 0.001) compared with 249 +/- 204 in the palmitic Acid period (P less than 0.001) and 236 +/- 201 in the oleic Acid period (NS).(ABSTRACT TRUNCATED AT 250 WORDS)