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Section: Physiology Download (pdf, 2.1MB )UDC612.395.5AuthorsSvetlana I. Malyavskaya*, Galina N. Kostrova*, Andrey V. Lebedev*, Natal’ya I. Belova**Northern (Arctic) Federal University named after M.V. Lomonosov (Arkhangelsk, Russian Federation) AbstractThe main marker of systemic inflammatory response is C-reactive protein (CRP), which plays a leading role in atherogenesis and the development of negative effects in vascular inflammation. CRP activity depends on genetic polymorphisms, of greatest practical interest being the single-nucleotide C3872T polymorphism of CRP gene, in which C allele carriers have higher CRP concentrations in the blood. The level of systemic inflammation is influenced by environmental factors, one of them being vitamin D, which can reduce the level of pro-inflammatory and increase the level of anti-inflammatory cytokines. Low vitamin D values in inflammatory diseases can probably be explained by the fact that inflammation reduces the level of 25-hydroxyvitamin D due to its increased catabolism during oxidative stress, as a result of malfunction of the enzymes metabolizing vitamin D in the liver. The study involved young people living in Arkhangelsk. We analysed the levels of 25-hydroxyvitamin D and high-sensitivity peripheral blood CRP and determined C3872T polymorphism of CRP gene. Vitamin D deficiency was found in 28 subjects (23 %), its deficit in 42 subjects (34 %) and severe deficit in 13 subjects (11 %) from the sample. The overwhelming majority – 82 subjects (66 %) – had CRP concentrations below 1 mg/l, indicating a low level of inflammatory response. The results of the study showed that the heterozygous variant of C3872T gene is the most common in this sample. C allele carriers had higher CRP values than carriers of the minor allele T (Z = 6.784; p = 0.034). In the group with 25-hydroxyvitamin D concentration below 30 ng/ml, CRP level was statistically significantly higher than that in the group with normal 25-hydroxyvitamin D concentration (p = 0.007). This research demonstrated the significance of the genetic component and the nutritional factor for CRP level in the blood.Keywordshigh-sensitivity CRP, C3872T polymorphism of CRP gene, vitamin D, 25-(OH)-D, chronic systemic inflammationReferences1. Ross R. Atherosclerosis – an Inflammatory Disease. N. Engl. J. Med., 1999, vol. 340, no. 2, pp. 115–126.2. Khaki Khatibi F., Yaghoubi A., Zarghami N., Rahbani M., Babaie H. Evaluation of hs-CRP, Antioxidant Markers and MDA in Patients of Coronary Artery Disease (CAD) Containing Non-Smokers and Non-Diabetics. J. Cardiovasc. Thorac. Res., 2011, vol. 2, no. 4, pp. 13–18. 3. Blagodatskikh K.A., Nikitin A.G., Pushkov A.A., Blagodatskikh E.G., Osmolovskaya V.S., Aseycheva O.Yu., Baklanova T.N., Talyzin P.A., Tereshchenko S.N., Dzhaiani N.A., Akatova E.V., Glezer M.G., Galyavich A.S., Zakirova V.B., Koziolova N.A., Polyanskaya E.A., Yagoda A.V., Boeva O.I., Khorolets E.V., Shlyk S.V., Volkova E.G., Margaryan M.P., Guz’ I.O., Konstantinov V.O., Kalishevich N.B., Zateyshchikov D.A., Nosikov V.V. Polimorfnye markery G2667C, G3014A, C3872T, A5237G gena CRP i geneticheskaya predraspolozhennost’ k neblagopriyatnomu techeniyu ishemicheskoy bolezni serdtsa u bol’nykh, perenesshikh obostrenie ishemicheskoy bolezni serdtsa [Polymorphic Markers G2667C, G3014A, C3872T, A5237G оf CRP Gene and Genetic Association with Unfavourable Outcomes of Coronary Artery Disease in Patients with History of Acute Ischemic Heart Disease]. Meditsinskaya genetika, 2011, no. 4, pp. 3–9. 4. Wang G., Song G., Wang L., Gao F., Guo N., Zhang Y., Zhao N., Yin X. Analysis of the Correlation Between Adiponectin Gene Polymorphism and Metabolic Syndrome Incidence and Its Relationship with the Degree of Atherosclerosis in Patients. Exp. Ther. Med., 2017, vol. 14, no. 5, pp. 5002–5006. 5. Kolz M., Koenig W., Müller M., Andreani M., Greven S., Illig T., Khuseyinova N., Panagiotakos D., Pershagen G., Salomaa V., Sunyer J., Peters A. DNA Variants, Plasma Levels and Variability of C-Reactive Protein in Myocardial Infarction Survivors: Results from the AIRGENE Study. Eur. Heart J., 2007, vol. 29, no. 10, pp. 1250–1258. 6. Shen J., Arnett D.K., Parnell L.D., Peacock J.M., Lai C.Q., Hixson J.E., Tsai M.Y., Province M.A., Straka R.J., Ordovas J.M. Association of Common C-Reactive Protein (CRP) Gene Polymorphisms with Baseline Plasma CRP Levels and Fenofibrate Response: The GOLDN Study. Diabetes Care, 2008, vol. 31, no. 5, pp. 910–915. 7. Ridker P.M. From C-Reactive Protein to Interleukin-6 to Interleukin-1: Moving Upstream to Identify Novel Targets for Atheroprotection. Circ. Res., 2016, vol. 118, no. 1, pp. 145–156. 8. Liefaard M.C., Ligthart S., Vitezova A., Hofman A., Uitterlinden A.G., Kiefte-de Jong J.C., Franco O.H., Zillikens M.C., Dehghan A. Vitamin D and C-Reactive Protein: A Mendelian Randomization Study. PLoS One, 2015, vol. 10, no. 7. 9. Amer M., Qayyum R. Relation Between Serum 25-Hydroxyvitamin D and C-Reactive Protein in Asymptomatic Adults (from the Continuous National Health and Nutrition Examination Survey 2001 to 2006). Am. J. Cardiol., 2012, vol. 109, no. 2, pp. 226–230. 10. Chen N., Wan Z., Han S.F., Li B.Y., Zhang Z.L., Qin L.Q. Effect of Vitamin D Supplementation on the Level of Circulating High-Sensitivity C-Reactive Protein: A Meta-Analysis of Randomized Controlled Trials. Nutrients, 2014, vol. 6, no. 6, pp. 2206–2216. 11. Guillot X., Semerano L., Saidenberg-Kermanac’h N., Falgarone G., Boissier M.C. Vitamin D and Inflammation. Joint Bone Spine, 2010, vol. 77, no. 6, pp. 552–557. DOI: 10.1016/j.jbspin.2010.09.018 12. Holick M.F., Binkley N.C., Bischoff-Ferrari H.A., Gordon C.M., Hanley D.A., Heaney R.P., Murad M.H., Weaver C.M. Evaluation, Treatment, and Prevention of Vitamin D Deficiency: An Endocrine Society Clinical Practice Guideline. J. Clin. Endocrinol. Metab., 2011, vol. 96, no. 7, pp. 1911–1930. 13. Autier P., Boniol M., Pizot C., Mullie P. Vitamin D Status and Ill Health: A Systematic Review. Lancet Diabetes Endocrinol., 2014, vol. 2, no. 1, pp. 76–89. 14. Henriksen V.T., Rogers V.E., Rasmussen G.L., Trawick R.H., Momberger N.G., Aguirre D., Barker T. Pro-Inflammatory Cytokines Mediate the Decrease in Serum 25(OH)D Concentrations After Total Knee Arthroplasty? Med. Hypotheses, 2014, vol. 82, no. 2, pp. 134–137. 15. Mangge H., Weghuber D., Prassl R., Haara A., Schnedl W., Postolache T.T., Fuchs D. The Role of Vitamin D in Atherosclerosis Inflammation Revisited: More a Bystander Than a Player? Curr. Vasc. Pharmacol., 2015, vol. 13, no. 3, pp. 392–398. 16. Adorini L., Penna G. Control of Autoimmune Diseases by the Vitamin D Endocrine System. Nat. Clin. Pract. Rheumatol., 2008, vol. 4, no. 8, pp. 404–412. 17. Marcotorchino J., Gouranton E., Romier B., Tourniaire F., Astier J., Malezet C., Amiot M.J., Landrier J.F. Vitamin D Reduces the Inflammatory Response and Restores Glucose Uptake in Adipocytes. Mol. Nutr. Food Res., 2012, vol. 56, no. 12, pp. 1771–1782. 18. Aranow C. Vitamin D and the Immune System. J. Investig. Med., 2011, vol. 59, no. 6, pp. 881–886. 19. Danesh J., Whincup P., Walker M., Lennon L., Thomson A., Appleby P., Gallimore J.R., Pepys M.B. Low Grade Inflammation and Coronary Heart Disease: Prospective Study and Updated Meta-Analyses. BMJ, 2000, vol. 321, no. 7255, pp. 199–204. 20. Helfand M., Buckley D., Fleming C., Fu R., Freeman M., Humphrey L., Rogers K., Walker M. Screening for Intermediate Risk Factors for Coronary Heart Disease. Agency for Healthcare Research and Quality (US). 2009. PMID: 20722172 |
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