Influence of visceral obesity on the secretion of adipokines with epicardial adipocytes in patients with coronary heart disease


Cite item

Full Text

Abstract

Aim. To study adipokine-cytokine profile of epicardial adipocytes (EAT) and subcutaneous adipose tissue (SAT) in conjunction with the area of visceral adipose tissue (VAT), biochemical and clinical characteristics of patients with coronary heart disease. Materials and methods. Examined 84 patients (70 men and 14 women) with coronary artery disease. In fact the presence of visceral obesity (VO) the patients were divided into two groups. Patients VO the sampling of adipocytes of EAT and SAT, with subsequent cultivation and evaluation of adipokine and provospalitelna activity. Carried out the determination of carbohydrate and lipid metabolism, adipokine and pro-inflammatory status in the blood serum. Results and discussion. It was found that adipokine-cytokine profile of adipocytes of EAT and SAT differ. Adipocytes art of the disease on the background characterized by an increase IL-1, TNF-α, leptin-adiponectin relationships and a decrease in the content of protective factors: adiponectin and anti-inflammatory cytokine IL-10. While the SAT adipocytes was characterized by a decrease in the concentration of soluble receptor for leptin and the more pronounced leptinresistance, and the increase in proinflammatory cytokines was offset by the increase in the concentration of IL-10. The presence associated with multi-vessel coronary bed lesion, multifocal atherosclerosis, insulin resistance, atherogenic dyslipidemia, an imbalance of adipokines and markers of inflammation. So the value of the square VAT determined higher concentrations of leptin, TNF-α in adipocytes and serum, lipid and carbohydrate metabolism and a lower content of soluble receptor for leptin. Conclusion. Thus, the disease on the background of the status of the adipocytes of EAT characterized as a "metabolic inflammation", and may indicate the direct involvement of adipocytes in the pathogenesis of coronary artery disease, due to the formation of adipokine imbalance and the activation of proinflammatory reactions.

About the authors

O V Gruzdeva

Research Institute for Complex Issues of Cardiovascular Disease; Siberian State Medical University, Ministry of Health of Russia

Email: o_gruzdeva@mail.ru
д.м.н., зав. лаб. исследования гомеостаза отд. диагностики сердечно-сосудистых заболеваний НИИ КПССЗ, доц. каф. патологической физиологии, медицинской и клинической биохимии Кемеровского ГМУ Кемерово, Россия

A D Borodkina

S.V. Belyaev Kemerovo Regional Clinical Hospital, Regional Diabetological Center

врач-эндокринолог областного центра диабетологии Кемеровской ОКБ им. С.В. Беляева Кемерово, Россия

O E Akbasheva

Kemerovo State Medical Academy, Ministry of Health of Russia

д.м.н., проф. каф. биохимии и молекулярной биологии с курсом клинической лабораторной диагностики, зам. декана медико-биологического факультета Сибирского ГМУ Томск, Россия

Yu A Dileva

Research Institute for Complex Issues of Cardiovascular Disease

к.м.н., н.с. лаб. исследований гомеостаза отд. диагностики сердечно-сосудистых заболеваний НИИ КПССЗ; ORCID: 0000-0002-6890-3287 Кемерово, Россия

L V Antonova

Research Institute for Complex Issues of Cardiovascular Disease

к.м.н., зав. лаб. клеточных технологий отд. экспериментальной и клинической кардиологии НИИ КПССЗ; ORCID: 0000-0002-8874-0788 Кемерово, Россия

V G Matveeva

Research Institute for Complex Issues of Cardiovascular Disease

к.м.н., с.н.с. лаб. клеточных технологий отдела экспериментальной и клинической кардиологии НИИ КПССЗ; ORCID: 0000-0002-4146-3373 Кемерово, Россия

E G Uchasova

Research Institute for Complex Issues of Cardiovascular Disease

к.м.н., с.н.с. лаб. исследований гомеостаза отд. диагностики сердечно-сосудистых заболеваний НИИ КПССЗ; ORCID: 0000-0003-4321-8977 Кемерово, Россия

S V Ivanov

Research Institute for Complex Issues of Cardiovascular Disease

д.м.н., в.н.с. лаб. реконструктивной хирургии мультифокального атеросклероза отд. мультифокального атеросклероза НИИ КПССЗ Кемерово, Россия

E V Belik

Research Institute for Complex Issues of Cardiovascular Disease

м.н.с. лаб. исследований гомеостаза отдела диагностики сердечно-сосудистых заболеваний НИИ КПССЗ Кемерово, Россия

E V Fanaskova

Research Institute for Complex Issues of Cardiovascular Disease

зав. кабинетом трансфузионной терапии, м.н.с. лаб. исследований гомеостаза отд. диагностики сердечно-сосудистых заболеваний НИИ КПССЗ Кемерово, Россия

V N Karetnikova

Research Institute for Complex Issues of Cardiovascular Disease; Siberian State Medical University, Ministry of Health of Russia

д.м.н., проф., зав. лаб. патофизиологии мультифокального атеросклероза отдела мультифокального атеросклероза НИИ КПССЗ, проф. каф. кардиологии и сердечно-сосудистой хирургии Кемеровского ГМУ; ORCID: 0000-0002-9801-9839 Кемерово, Россия

A N Kokov

Research Institute for Complex Issues of Cardiovascular Disease

к.м.н., зав. лаб. рентгеновской и томографической диагностики НИИ КПССЗ; ORCID: 0000-0002-7573-0636 Кемерово, Россия

O L Barbarash

Research Institute for Complex Issues of Cardiovascular Disease; Siberian State Medical University, Ministry of Health of Russia

член-корр. РАН, д.м.н., проф., директор НИИ КПССЗ, зав. каф. кардиологии и сердечно-сосудистой хирургии Кемеровского ГМУ Кемерово, Россия

References

  1. Lozano R, Naghavi M, Foreman K, et al. Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: a systematic analysis for the Global Burden of Disease Study 2010. Lancet. 2012;380:2095-2128. doi: 10.1016/S0140-6736(12)61728-0
  2. Roth G.A, Forouzanfar M.H, Moran A.E, et al. Demographic and epidemiologic drivers of global cardiovascular mortality. N Engl J Med. 2015;372(14):1333-1341. doi: 10.1056/NEJMoa1406656
  3. Lainscak M, Blue L, Clark A.L, et al. Self - care management of heart failure: practical recommendations from the Patient Care Committee of the Heart Fail - ure Association of the European Society of Cardiology. Eur J Heart Failure. 2011;13(2):115-126. doi: 10.1093/eurjhf/hfq219
  4. Veilleux A, Cote J.A, Blouin K, et al. Glucocorticoid - induced androgen inactivation by aldo - keto reductase 1C2 promotes adipogenesis in human preadipocytes. Am J Physiol Endocrinol Metab. 2012;302:E941-941. doi: 10.1007/978-1-4614-0965-6_5
  5. Silva A.A, Carmo J.M, Dubinion J, et al. Obesity - induced hypertension: role of sympathetic nervous system, leptin, and melanocortins. J Biol Chem. 2010;285(23):17271-17276. doi: 10.1074/jbc.R110.113175
  6. Bergman R.N, Kim S.P, Catalano K.J, et al. Why visceral fat is bad: mechanisms of the metabolic syndrome. Obesity (Silver Spring). 2006;14(Suppl 1):16S-19S. doi: 10.1038/oby.2006.277
  7. Iacobellis G, Corradi D, Sharma A.M. Epicardial adipose tissue: anatomic, biomolecular and clinical relationships with the heart. Nat Clin Pract Cardiovasc Med. 2005;2:536-543. doi: 10.1038/ncpcardio0319
  8. Britton K.A, Fox C.S. Ectopic fat depots and cardiovascular disease. Circulation. 2011;124.(24):e837-e841. doi: 10.1161/circulationaha.111.077602
  9. Sjoestrom L. A computed tomography based multicompartment body composition technique and anthropometric predictions of lean body mass, total and subcutaneous adipose tissue. Int J Obes. 1991;15:19-30.
  10. Carswell K.A, Lee M, Fried S.K. Culture of Isolated Human Adipocytes and Isolated Adipose Tissue. Methods Mol Biol. 2012;806:203-214. doi: 10.1007/978-1-61779-367-7_14
  11. Suga H, Matsumoto D, Inoue K et al. Numerical Measurement of Viable and Nonviable Adipocytes and Other Cellular Components in Aspirated Fat Tissue. Plast Reconstr Surg. 2008;122(1):103-114. doi: 10.1097/PRS.0b013e31817742ed
  12. Matthews D.R, Hosker J.P, Rudenski A.S, et al. Homeostasis model assessment: insulin resistance and beta - cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia. 1985;28:412-419. doi: 10.1007/BF00280883
  13. Misra M, Miller K.K, Almazan C, еt al. Hormonal and body composition predictors of soluble leptin receptor, leptin, and free leptin index in adolescent girls with anorexia nervosa and controls and relation to insulin sensitivity. J Clin Endocrinol Metab. 2004;89(7):3486-3495. doi: 10.1210/jc.2003-032251
  14. Отт А.В., Чумакова Г.А., Веселовская Н.Г. Значение лептинорезистентности в развитии различных метаболических фенотипов ожирения. Российский кардиологический журнал. 2016;(4):4-18. doi: 10.15829/1560-4071-2016-4-14-18
  15. Mahabadi A.A, Massaro J.M, Rosito G.A, et al. Association of pericardial fat, intrathoracic fat, and visceral abdominal fat with cardiovascular disease burden: The Framingham Heart Study. Eur Heart J. 2009;30:850-856. doi: 10.1093/eurheartj/ehn573
  16. Jeong J.W, Jeong M.H, Yun K.H, et al. Echocardiographic epicardial fat thickness and coronary artery disease. Circ J. 2007;71:536-539. doi: 10.1253/circj.71.536
  17. Donoso M.A, Muñoz-Calvo M.T, Barrios V et al. Increased leptin/adiponectin ratio and free leptin index are markers of insulin resistance in obese girls during pubertal development. Hormone Res Paediatr. 2013;80(5):363-370. doi: 10.1159/000356046
  18. Libby P, Ridker P.M, Maseri A. Inflammation and atherosclerosis. Circulation. 2002;105:1135-1143.
  19. Chia S, Quadan M, Newton R, et al. Intra - arterial tumor necrosis factor - alpha impairs endothelial - dependent dilatation in humans. Arterioscler Thromb Vasc Biol. 2003;23:695-701.
  20. Lima M.M, Pareja J.C, Alegre S.M, et al. Visceral fat resection in humans: effect on insulin sensitivity, beta - cell function, adipokines, and inflammatory markers. Obesity (Silver Spring). 2013;21(3):E182-189. doi: 10.1002/oby.20030

Copyright (c) 2018 Consilium Medicum

Creative Commons License
This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License.
 
 


This website uses cookies

You consent to our cookies if you continue to use our website.

About Cookies