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The effect of different individual TFA isomers on cardiovascular disease (CVD) has been a limited study, especially for stroke. We aimed to investigate the relationships between four major plasma TFA isomer (elaidic, vaccenic, palmitelaidic and linolelaidic acid) concentrations and the risk of CVD, stroke and non-stroke CVD. A cross-sectional study was conducted, utilising a nationally representative sample of US adults in the National Health and Nutrition Examination Survey. Among the 3504 participants, 304 participants self-reported CVD history. The highest quintile of elaidic acid intake was associated with a 233% higher CVD risk (p = .010). Adjusted for age, gender and race, palmitelaidic acid was associated with a decreased CVD risk, but the effect size was diminished in a subsequent analysis model. For stroke risk, we failed to identify any associations. In addition to elaidic acid, the health effect of palmitelaidic acid should be paid more attention in the future studies. [ABSTRACT FROM AUTHOR]

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 9 t12 t18:2 induced a stronger lesion effect on HUVECs compared with 9 t18:1 through lipid rafts, which indicated that we should pay attention to 9 t12 t18:2 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. [ABSTRACT FROM AUTHOR]