Dietary intake of trans fatty acids and systemic inflammation in women. (1/153)

BACKGROUND: trans Fatty acid (TFA) intake predicts risks of coronary artery disease and diabetes. Systemic inflammation may be involved in the pathogenesis of such conditions; however, relations between TFA intake and systemic inflammation are not well established. OBJECTIVE: We investigated the relations between TFA intake and inflammatory markers. DESIGN: In 823 generally healthy women in the Nurses' Health Study I and II, concentrations of soluble tumor necrosis factor alpha receptors 1 and 2 (sTNF-R1, sTNF-R2), interleukin 6 (IL-6), and C-reactive protein (CRP) were measured. Usual dietary intakes assessed from 2 semiquantitative food-frequency questionnaires were averaged for each subject. RESULTS: In age-adjusted analyses, TFA intake was positively associated with sTNF-R1 and sTNF-R2 (P for trend < 0.001 for each): sTNF-R1 and sTNF-R2 concentrations were 10% (+108 pg/mL; 95% CI: 50, 167 pg/mL) and 12% (+258 pg/mL; 138, 377 pg/mL) higher, respectively, in the highest intake quintile than in the lowest. These associations were not appreciably altered by adjustment for body mass index, smoking, physical activity, aspirin and nonsteroidal antiinflammatory drug use, alcohol consumption, and intakes of saturated fat, protein, n-6 and n-3 fatty acids, fiber, and total energy. Adjustment for serum lipid concentrations partly attenuated these associations, which suggests that they may be partly mediated by effects of TFAs on serum lipids. TFA intake was not associated with IL-6 or CRP concentrations overall but was positively associated with IL-6 and CRP in women with higher body mass index (P for interaction = 0.03 for each). CONCLUSIONS: TFA intake is positively associated with markers of systemic inflammation in women. Further investigation of the influences of TFAs on inflammation and of implications for coronary disease, diabetes, and other conditions is warranted.  (+info)

Trans fatty acids in adipose tissue and the food supply are associated with myocardial infarction. (2/153)

Metabolic studies have clearly shown that trans fatty acids (TFAs) elevate LDL and lower HDL cholesterol. Epidemiologic studies showed a relation between TFA intake and the risk of myocardial infarction (MI), but studies examining adipose tissue TFAs have not uniformly confirmed this. We performed a case control study examining both adipose tissue levels and dietary intake of TFAs and first MI. Between 1995 and 1997, 209 cases of first MI completed a 300-item FFQ and 79 had an adipose tissue biopsy; 179 matched controls completed the FFQ and 167 had a biopsy. During the course of the study (mid-1996), TFAs were eliminated from margarines sold in Australia. Cases biopsied before mid-1996 had greater levels of trans 18:1(n-9) (32% P < 0.03) and trans 18:1(n-11) (23%, P < 0.001) than controls biopsied before mid-1996. After June 1996, there were no differences between cases and controls in any of the adipose tissue TFAs measured. Logistic regression showed that trans 18:1(n-11) (P = 0.03) was an independent predictor of a first MI. Cases consumed 0.5 g/d (P = 0.002) more TFAs than controls. Subjects in the highest quintile of TFA intake had an OR for first MI of 2.1 (95% CI, 1.1-4.3), which was not independent of saturated fat intake. Apparent TFA intake from margarine was related to adipose tissue 18:1t[(n-9) and (n-10)] in 1995 (r = 0.66, 0.66, respectively). We conclude that TFAs in adipose tissue are associated with an increased risk of coronary artery disease and rapidly disappear from adipose tissue when not included in margarines.  (+info)

Dietary hydrogenated fat increases high-density lipoprotein apoA-I catabolism and decreases low-density lipoprotein apoB-100 catabolism in hypercholesterolemic women. (3/153)

OBJECTIVE: To determine mechanisms contributing to decreased high-density lipoprotein cholesterol (HDL-C) and increased low-density lipoprotein cholesterol (LDL-C) concentrations associated with hydrogenated fat intake, kinetic studies of apoA-I, apoB-100, and apoB-48 were conducted using stable isotopes. METHODS AND RESULTS: Eight postmenopausal hypercholesterolemic women were provided in random order with 3 diets for 5-week periods. Two-thirds of the fat was soybean oil (unsaturated fat), stick margarine (hydrogenated fat), or butter (saturated fat). Total and LDL-C levels were highest after the saturated diet (P<0.05; saturated versus unsaturated) whereas HDL-C levels were lowest after the hydrogenated diet (P<0.05; hydrogenated versus saturated). Plasma apoA-I levels and pool size (PS) were lower, whereas apoA-I fractional catabolic rate (FCR) was higher after the hydrogenated relative to the saturated diet (P<0.05). LDL apoB-100 levels and PS were significantly higher, whereas LDL apoB-100 FCR was lower with the saturated and hydrogenated relative to the unsaturated diet. There was no significant difference among diets in apoA-I or B-100 production rates or apoB-48 kinetic parameters. HDL-C concentrations were negatively associated with apoA-I FCR (r=-0.56, P=0.03) and LDL-C concentrations were negatively correlated with LDL apoB-100 FCR (r=-0.48, P=0.05). CONCLUSIONS: The mechanism for the adverse lipoprotein profile observed with hydrogenated fat intake is determined in part by increased apoA-I and decreased LDL apoB-100 catabolism.  (+info)

Dietary fatty acids affect plasma markers of inflammation in healthy men fed controlled diets: a randomized crossover study. (4/153)

BACKGROUND: The effect of individual dietary fatty acids on emerging risk factors for cardiovascular disease that are associated with subclinical inflammation is unknown. OBJECTIVE: The goal was to evaluate the role of dietary fat and specific fatty acids, especially trans fatty acids, in altering concentrations of markers of inflammation in humans fed controlled diets. DESIGN: In a randomized crossover design, 50 men consumed controlled diets for 5 wk that provided 15% of energy from protein, 39% of energy from fat, and 46% of energy from carbohydrate. Eight percent of fat or fatty acids was replaced across diets with the following: cholesterol, oleic acid, trans fatty acids (TFAs), stearic acid (STE), TFA+STE (4% of energy each), and 12:0-16:0 saturated fatty acids (LMP). RESULTS: Fibrinogen concentrations were higher after consumption of the diet enriched in stearic acid than after consumption of the carbohydrate diet. C-reactive protein concentrations were higher after consumption of the TFA diet than after consumption of the carbohydrate diet, but were not significantly different after consumption of the TFA and TFA+STE diets than after consumption of the LMP diet. Interleukin 6 concentrations were lower after consumption of the oleic acid diet than after consumption of the LMP, TFA, and STE diets. E-selectin concentrations were higher after consumption of the TFA diet than after consumption of the carbohydrate diet. Consumption of the TFA but not the TFA+STE diet resulted in higher E-selectin concentrations than did the LMP diet. CONCLUSIONS: These data provide evidence that dietary fatty acids can modulate markers of inflammation. Although stearic acid minimally affects LDL cholesterol, it does appear to increase fibrinogen concentrations.  (+info)

Conjugated linoleic acid isomers and trans fatty acids inhibit fatty acid transport in hepatoma 7288CTC and inguinal fat pads in Buffalo rats. (5/153)

Conjugated linoleic acid (CLA) and some trans fatty acids (FA) decrease tumor growth and alter tumor and host lipid uptake and storage. The goal of this study was to test the hypothesis that the acute inhibitory effects of CLA isomers and trans FAs on FA transport in tumors and white adipose tissue are mediated via an inhibitory G-protein coupled (GPC), FFA receptor (FFAR). Experiments were performed in hepatoma 7288CTC and inguinal fat pads in Buffalo rats during perfusion in situ. CLA isomers and trans FAs (0.03-0.4 mmol/L, in plasma) were added to the arterial blood, and FA uptake or release was measured by arterial minus venous difference. In hepatoma 7288CTC, the CLA isomers, t10,c12-CLA > (+/-)-9-HODE [13-(S)-hydroxyoctadecadienoic acid] > t9,t11-CLA, and the trans FAs, linolelaidic = vaccenic > elaidic, decreased cAMP content and inhibited FA uptake, 13(S)-HODE release, extracellular signal-regulated kinase p44/p42 phosphorylation, and [(3)H]thymidine incorporation. Other CLA isomers, c9,t11-CLA, 13-(S)-HODE, c9,c11-CLA, and c11,t13-CLA, had no effect. In inguinal fat pads, FA transport was inhibited by t10,c12-CLA = linolelaidic acid > trans vaccenic acid, whereas c9,t11-CLA had no effect. In both hepatoma 7288CTC and inguinal fat pad, addition of either pertussis toxin or 8-Br-cAMP to the arterial blood reversed the inhibitions of FA transport. These results support the idea that an inhibitory GPC FFAR reduces cAMP and controls FA transport by CLA isomers and trans FAs. Ligand activity is conferred by the presence of a trans double bond proximal to the carboxyl group.  (+info)

Plasma cholesteryl esters provided by lecithin:cholesterol acyltransferase and acyl-coenzyme a:cholesterol acyltransferase 2 have opposite atherosclerotic potential. (6/153)

Evidence suggests that ACAT2 is a proatherogenic enzyme that contributes cholesteryl esters (CEs) to apoB-containing lipoproteins, whereas LCAT is an antiatherogenic enzyme that facilitates reverse cholesterol transport by esterifying free cholesterol on HDL particles. We hypothesized that deletion of LCAT and ACAT2 would lead to absence of plasma CEs and reduced atherosclerosis. To test this hypothesis, ACAT2-/- LCAT-/- LDLr-/-, ACAT2-/- LDLr-/-, and LCAT-/- LDLr-/- mice were fed a 0.15% cholesterol diet for 20 weeks. In comparison to LDLr-/- mice, the total plasma cholesterol (TPC) of ACAT2-/- LCAT-/- LDLr-/- mice was 67% lower because of the complete absence of plasma CEs, leading to 94% less CE accumulation in the aorta. In the LCAT-/- LDLr-/- mice, TPC and atherosclerosis were significantly higher because of increased accumulations of ACAT2-derived CE. In ACAT2-/- LDLr-/- mice, again compared with LDLr-/- mice, TPC was 19% lower, whereas atherosclerosis was 88% lower. Therefore, the absence of ACAT2 led to a significant reduction in TPC although benefits in reduction of atherosclerosis were much more pronounced. Overall, the data suggest that ACAT2-derived CE is the predominant atherogenic lipid in blood, and that an important goal for prevention of atherosclerosis is to limit ACAT2-derived CE accumulation in lipoproteins.  (+info)

trans fatty acids and systemic inflammation in heart failure. (7/153)

BACKGROUND: trans fatty acid (TFA) intake increases systemic inflammation in healthy persons. However, the effect in patients with established heart disease is unknown. OBJECTIVE: Our aim was to determine whether TFAs are associated with systemic inflammation in patients with established heart disease. DESIGN: Red blood cell membrane TFAs, a biomarker of dietary intake, and inflammatory marker concentrations were ascertained in 86 ambulatory patients with established heart failure. Associations between TFA levels and inflammatory markers were evaluated by linear regression. RESULTS: Mean (+/-SD) TFA levels were 1.8 +/- 0.4% of membrane fatty acids (range: 0.7-2.9%). For each inflammatory marker, associations are presented as the absolute difference and percentage difference from the mean for each 1% higher membrane TFA level. After adjustment for age, sex, body mass index, diabetes, smoking, ejection fraction, New York Heart Association class, ischemic etiology, statin use, and serum glucose, TFA levels were positively associated with interleukin (IL) 1beta (difference from mean: 0.38 pg/mL; percentage difference from mean: 66%; P=0.04), IL-1 receptor antagonist (4033 pg/mL; 297%; P=0.006), IL-6 (9.5 pg/mL; 123%; P=0.006), IL-10 (241 pg/mL; 183%; P=0.02), tumor necrosis factor (TNF) alpha (256 pg/mL; 249%; P=0.02), TNF receptor 1 (537 pg/mL; 41%; P=0.03), TNF receptor 2 (39 242 pg/mL; 247%; P=0.001), monocyte chemoattractant protein 1 (117 pg/mL; 119%; P=0.004), and brain natriuretic peptide (40 pg/mL; 57%; P=0.04). Further adjustments for other patient characteristics did not significantly alter the results. CONCLUSION: TFAs are strongly associated with systemic inflammation in patients with heart disease, which suggests that attention to TFA intake may be important for secondary prevention efforts.  (+info)

Consumption of trans fatty acids is related to plasma biomarkers of inflammation and endothelial dysfunction. (8/153)

Trans fatty acid intake has been associated with a higher risk of cardiovascular disease. The relation is explained only partially by the adverse effect of these fatty acids on the lipid profile. We examined whether trans fatty acid intake could also affect biomarkers of inflammation and endothelial dysfunction including C-reactive protein (CRP), interleukin-6 (IL-6), soluble tumor necrosis factor receptor 2 (sTNFR-2), E-selectin, and soluble cell adhesion molecules (sICAM-1 and sVCAM-1). We conducted a cross-sectional study of 730 women from the Nurses' Health Study I cohort, aged 43-69 y, free of cardiovascular disease, cancer, and diabetes at time of blood draw (1989-1990). Dietary intake was assessed by a validated FFQ in 1986 and 1990. CRP levels were 73% higher among those in the highest quintile of trans fat intake, compared with the lowest quintile. IL-6 levels were 17% higher, sTNFR-2 5%, E-selectin 20%, sICAM-1 10%, and sVCAM-1 levels 10% higher. Trans fatty acid intake was positively related to plasma concentration of CRP (P = 0.009), sTNFR-2 (P = 0.002), E-selectin (P = 0.003), sICAM-1 (P = 0.007), and sVCAM-1 (P = 0.001) in linear regression models after controlling for age, BMI, physical activity, smoking status, alcohol consumption, intake of monounsaturated, polyunsaturated, and saturated fatty acids, and postmenopausal hormone therapy. In conclusion, this study suggests that higher intake of trans fatty acids could adversely affect endothelial function, which might partially explain why the positive relation between trans fat and cardiovascular risk is greater than one would predict based solely on its adverse effects on lipids.  (+info)