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RELATION OF METABOLIC SYNDROME C-REACTIVE PROTEIN FIBRINOGEN
E.S. Eren 1 , F.A. Oner 2 , M.E. Pi¸sKinpa¸sa 2 , M. Erguney 2 . 1 Internal Medicine, Dr. Burhan Nalbantoˇglu Hospital/lefko¸sa, Turkish Republic of North Cyprus; 2 Clinic of Internal Medicine, Istanbul Education and Research HospITal, Istanbul, Turkey Aims: Purpose of our study is to determine the correlation of serum levels of CRP and fibrinogen with the other components of Metabolic syndrome (MS) and in that way to prove that this can be a simple and reliable method for the prediction of increased coronary heart disease risk. Material and methods: The study population consisted of 50 patients (31 women, 19 men) from, our hospital’s general medicine practice, who were free of any known chronic illnesses and carry at least three of MS criterias. Blood collections of all these 50 patients were used for assay of fasting blood glucose, triglycerides, HDL- cholesterol, CRP and fibrinogen levels. Waist circumference is measured in all patients, and blood pressures are measured in supine position after 10 minutes rest from right arm twice and the mean value is taken into consideration. Results: Our findings show that CRP and fibrinogen levels are significantly high in patients with MS. Particularly, there is a significant correlation between CRP levels-waist circumference and fibrinogen levels-fasting blood glucose. Conclusion: Chronic subclinic inflammation is one of the pathophysiological mechanisms expressing the increased atherosclerotic disease risk related with MS. We can have a simple and reliable method for prediction and treatment of atherosclerotic disease by estimating the level of serum CRP and fibrinogen which are chronic inflammatory mediators. 2
TWO SNPS OF ENDOTHELIAL NITRIC OXIDE SYNTHASE GENE (E298D AND I19342) REGULATE POSTPRANDIAL VASCULAR REACTIVITY
Background and Aims: Endothelial Nitric Oxide Synthase (eNOS) regulates the formation of Nitric Oxide, the main endothelial antioxidant. E298d and i19342 single nucleotide polymorphisms (SNPs) of eNOS gene are potential functional SNPs controlling eNOS metabolism, by their gene location. We investigated the effects of e298d and i19342 SNPs on the postprandial microvascular endothelial function (MEF) after a fatty meal. Methods: Forty healthy young males, ingested a meal containing 1gr fat/kg, 60.000 UI of vitamin A per m2 and 7mgr of cholesterol/kg (60% fat, 15% proteins and 25% carbohydrates). MEF was assessed with laser-doppler flowmetry at baseline and 2, 4, 6 and 8 hours after the meal. Isolated and combined (haplotype) effects of the SNPs were studied by ANOVA. Results: Postprandial MEF was impaired in the carriers of minor alleles of the SNPs (global mean 60,99 VS 87,25, p=0,016 for i19342; 63,62 VS 95,71, p=0,011 for e298d) with significant differences at time-points 4h, 6h, and 8h. Additive negative effects of the haplotype corresponding
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PREVENTION AND REGRESSIVE EFFECTS OF STATIN AGAINST ATHEROSCLEROTIC CHANGES IN HYPERTENSIVE RAT CAROTID ARTERIES
K. Abe, A. Tsuchiya, S. Nagotani, K. Deguchi, T. Yamashita, Y. Ikeda, T. Kamiya. Department of Neurology, Okayama University, Okayama city, Japan The exact mechanism of stroke prevention by statins (HMG-CoA reductase inhibitors) in human patients is not fully understood. In order to address this issue, spontaneously hypertensive rats (SHR-SP) were fed high cholestherol diet for 4w from 8 to 12w of age with simvastatin orally administered for the same 4w or later 2w during this period. Their common carotid arteries at 12w of age showed an intensive lipid deposition and strong stainings of LOX-1, MCP-1, and Iba-1 in carotid endothelium of the vehicle group, while lesser depositions and stainings in the whole 4w and the later 2w treated groups. These results suggest that the high cholesterol diet rapidly and strongly causes atherosclerotic change in carotid arteries of SHR-SP, and that the treatment with statin prevents (4w group) and even partially regresses (later 2w group) such a carotid atherosclerotic change, explaining a part of mechanisms of human stroke prevention by statins. 4
HAZELNUT CONSUMPTION PROTECT LOW DENSITY LIPOPROTEIN (LDL) AGAINST OXIDATION AND DECREASE PLASMA OXIDAZED LDL LEVEL
A. Orem 1 , F. Balaban 1 , B.V. Kural 1 , C. Orem 2 , I. Turhan 1 . 1 Biochemistry, KTU, Medical Faculty, Trabzon, Turkey; 2 Cardiology, KTU, Medical Faculty Backgrounds and aims: Nuts consumption had beneficial effects on protection for development of atherosclerotic process. We determine the effects of hazelnut-enriched diet on atherogenic tendency of LDL by evaluating susceptibility of LDL to oxidation by using t-lag, α-tocopherol content of LDL and plasma ox-LDL, lipid and lipoprotein levels in subjects with normolipidemic healthy subjects. Methods and results: Twenty-one healthy individuals (13 women and 8 men) with a mean age 28±5 years were included in this study. During to 4 weeks study period, 1 g/kg/day hazelnut was added to theirs habitual daily diets. This increased 122% of the ratio of monounsaturated fatty acids/saturated fatty acids. Blood sample were evaluated at baseline, 15th and 30th day. t-lag and α-tocopherol content of LDL were found to be increased while ox-LDL levels decreased during the study period. Ox-LDL levels in baseline, 15th day and 30th day were correlated with t-lags (r = 0.52, p<0.05; r = - 0.50, p<0.05; r = - 0.35, p=0.12, respectively). Total cholesterol, LDL-cholesterol, apo B and apo B/apo AI ratio were found to be significantly lower while apo AI were higher. Conclusions: Because of high monounsaturated fatty acid and vitamin E content of hazelnut-enriched diet, it may play important role to decrease atherogenic tendency of LDL by decreasing susceptibility of LDL to oxidation and plasma ox-LDL levels and beyond its beneficial effect on lipid and lipoprotein levels.
77th Congress of the European Atherosclerosis Society, April 26–29, 2008, Istanbul, Turkey
PUBLICATION ONLY
J. Delgado-Lista 1 , P. Perez-Martinez 1 , J. Mattei 2 , Y. Jimenez 1 , F. Fuentes 1 , C. Marin 1 , L.D. Parnell 2 , J.M. Ordovas 2 , F. Perez-Jimenez 1 , J. Lopez-Miranda 1 . 1 Lipids and Atherosclerosis Unit/Reina Sofia University Hospital, Cordoba, Spain; 2 Nutrition and Genomics Lab/HNRCA At TUFTS University, Boston, MA, USA
to double mutant carrier (haplotype 22) were found as compared with the haplotype without mutant alleles (haplotype 11) (global mean 60,99 VS 95,70 p=0,005). Conclusions: Carriers of minor allele for e298d and i19342 have an impaired postprandial MEF. Double carriers are specially at high risk for coronary events in the postprandial state due to an impaired MEF.