Plasma adiponectin as a predictor of the effectiveness of coronary heart disease therapy in patients with metabolic syndrome

Cover Page

Cite item

Full Text

Open Access Open Access
Restricted Access Access granted
Restricted Access Subscription Access

Abstract

BACKGROUND: Adiponectin, an adipose tissue protein, plays a crucial role in the development of metabolic syndrome and atherosclerosis. As a potential therapeutic target, this adipokine can be considered in the context of treatment strategies.

AIM: The aim of this study was to assess the correlation between changes in plasma adiponectin concentration during coronary heart disease therapy and the effectiveness of the treatment, as well as to examine the relationship between initial adiponectin levels and treatment outcomes in patients with metabolic syndrome.

MATERIALS AND METHODS: The study included 31 patients with coronary heart disease and metabolic syndrome (age 59.7 ± 5.9 years, 21 women) which underwent the reexamination after 2–3 years. Most patients received statins (n = 26), while some received fibrates (n = 4) and hypoglycemic drugs (n = 4). Additionally, the patients were on hypotensive and antithrombotic therapies. The effectiveness of coronary heart disease therapy was assessed by evaluating changes in the functional class of angina pectoris and exercise tolerance measured through cycle ergometry. Plasma samples were collected at the initial and reexamination periods to determine glucose, insulin, adiponectin, leptin, and lipidogram parameters.

RESULTS: The study revealed improvements in insulin sensitivity and plasma lipid spectrum, along with reduced levels of plasma leptin and increased adiponectin levels during the course of therapy. In addition, some patients showed enhanced exercise tolerance. Among the biochemical parameters, changes in insulin resistance during therapy correlated with improvements in exercise performance indicators during cycle ergometry (r = −0.32…−0.36, p < 0.05). Moreover, multiple regression analysis indicated that the initial adiponectin concentration independently determined changes in inotropic reserve and the amount of work performed (β = 0.44, p = 0.04 and β = 0.64, p = 0.008).

CONCLUSIONS: The study’s findings regarding the association of plasma adiponectin concentration with changes in exercise tolerance during coronary heart disease therapy suggest the potential for developing specific approaches to raise adiponectin levels in the future.

About the authors

Elvira M. Firova

Institute of Experimental Medicine

Email: firova@yandex.ru

Cand. Sci. (Med.), head of the Cardiology Department of the Clinic

Russian Federation, Saint Petersburg

Dmitry A. Tanyanskiy

Institute of Experimental Medicine

Author for correspondence.
Email: dmitry.athero@gmail.com
ORCID iD: 0000-0002-5321-8834
SPIN-code: 9303-9445

Dr. Sci. (Med.), head of the Biochemistry Department

Russian Federation, Saint Petersburg

References

  1. Bershtein LL. New possibilities to reduce the residual risk in patients with ischemic heart disease. Kardiologiia. 2020;60(11): 110–116. (In Russ.) doi: 10.18087/cardio.2020.11.n1370
  2. Kern PA, Di Gregorio GB, Lu T, et al. Adiponectin expression from human adipose tissue: relation to obesity, insulin resistance, and tumor necrosis factor-alpha expression. Diabetes. 2003;52(7): 1779–1785. doi: 10.2337/diabetes.52.7.1779
  3. Razgildina ND, Brovin DL, Pobozheva IA, et al. Adiponectine gene expression in subcutaneous and intra-abdominal adipose tissue in women with varying degrees of obesity. Tsitologiya. 2018;60(7): 531–535. (In Russ.) doi: 10.31116/tsitol.2018.07.08
  4. Tschritter O, Fritsche A, Thamer C, et al. Plasma adiponectin concentrations predict insulin sensitivity of both glucose and lipid metabolism. Diabetes. 2003;52(2):239–243. doi: 10.2337/diabetes.52.2.239
  5. Tanyansky DA, Firova EM, Shatilina LV, Denisenko AD. Adiponectin: lowering in metabolic syndrome and independent relation to hypertriglyceridemia. Kardiologiia. 2008;48(12):20–25. (In Russ.)
  6. Yamauchi T, Nio Y, Maki T, et al. Targeted disruption of AdipoR1 and AdipoR2 causes abrogation of adiponectin binding and metabolic actions. Nat Med. 2007;13:332–339. doi: 10.1038/nm1557
  7. Ma Y, Liu D. Hydrodynamic delivery of adiponectin and adiponectin receptor 2 gene blocks high-fat diet-induced obesity and insulin resistance. Gene Ther. 2013;20(8):846–852. doi: 10.1038/gt.2013.8
  8. Folco EJ, Rocha VZ, Lopez-Ilasaca M, Libby P. Adiponectin inhibits pro-inflammatory signaling in human macrophages independent of interleukin-10. J Biol Chem. 2009;284(38):25569–25575. doi: 10.1074/jbc.M109.019786
  9. Wang Y, Wang X, Lau WB, et al. Adiponectin inhibits tumor necrosis factor-α-induced vascular inflammatory response via caveolin-mediated ceramidase recruitment and activation. Circ Res. 2014;114(5):792–805. doi: 10.1161/CIRCRESAHA.114.302439
  10. Ouchi N, Kihara S, Arita Y, et al. Adipocyte-derived plasma protein, adiponectin, suppresses lipid accumulation and class A scavenger receptor expression in human monocyte-derived macrophages. Circulation. 2001;103(8):1057–1063. doi: 10.1161/01.cir.103.8.1057
  11. Motobayashi Y, Izawa-Ishizawa Y, Ishizawa K, et al. Adiponectin inhibits insulin-like growth factor-1-induced cell migration by the suppression of extracellular signal-regulated kinase 1/2 activation, but not Akt in vascular smooth muscle cells. Hypertens Res. 2009;32:188–193. doi: 10.1038/hr.2008.19
  12. Zhang W, Shu C, Li Q, et al. Adiponectin affects vascular smooth muscle cell proliferation and apoptosis through modulation of the mitofusin-2-mediated Ras-Raf-Erk1/2 signaling pathway. Mol Med Rep. 2015;12(3):4703–4707. doi: 10.3892/mmr.2015.3899
  13. Adya R, Tan BK, Chen J, Randeva HS. Protective actions of globular and full-length adiponectin on human endothelial cells: novel insights into adiponectin-induced angiogenesis. J Vasc Res. 2012;49:534–543. doi: 10.1159/000338279
  14. Saneipour M, Ghatreh-Samani K, Heydarian E, et al. Adiponectin inhibits oxidized low density lipoprotein-induced increase in matrix metalloproteinase 9 expression in vascular smooth muscle cells. ARYA Atheroscler. 2015;11(3):191–195.
  15. Tanyanskiy DA, Pigarevsky PV, Maltseva SV, et al. Adiponectin in normal and atherosclerotic intima of human aorta. Arkhiv Patologii. 2022;84(6):16–22. (In Russ.) doi: 10.17116/patol20228406116
  16. Bang OY, Saver JL, Ovbiagele B, et al. Adiponectin levels in patients with intracranial atherosclerosis. Neurology. 2007;68(22): 1931–1937. doi: 10.1212/01.wnl.0000263186.20988.9f
  17. Wang Y, Zheng A, Yan Y, et al. Association between HMW adiponectin, HMW-total adiponectin ratio and early-onset coronary artery disease in Chinese population. Atherosclerosis. 2014;235(2):392–397. doi: 10.1016/j.atherosclerosis.2014.05.910
  18. Sook Lee E, Park S-s, Kim E, et al. Association between adiponectin levels and coronary heart disease and mortality: a systematic review and meta-analysis. Int J Epidemiol. 2013;42(4):1029–1039. doi: 10.1093/ije/dyt087
  19. Wu Z-J, Cheng Y-J, Gu W-J, Aung LHH. Adiponectin is associated with increased mortality in patients with already established cardiovascular disease: a systematic review and meta-analysis. Metabolism. 2014;63(9):1157–1166. doi: 10.1016/j.metabol.2014.05.001
  20. Christiansen T, Paulsen SK, Bruun JM, et al. Exercise training versus diet-induced weight-loss on metabolic risk factors and inflammatory markers in obese subjects: a 12-week randomized intervention study. Am J Physiol Endocrinol Metab. 2010;298(4): E824–E831. doi: 10.1152/ajpendo.00574.2009
  21. Chruściel P, Sahebkar A, Rembek-Wieliczko M, et al. Lipid and Blood Pressure Meta-analysis Collaboration (LBPMC) Group. Impact of statin therapy on plasma adiponectin concentrations: A systematic review and meta-analysis of 43 randomized controlled trial arms. Atherosclerosis. 2016;253:194–208. doi: 10.1016/j.atherosclerosis.2016.07.897
  22. Sharma PK, Bhansali A, Sialy R, et al. Effects of pioglitazone and metformin on plasma adiponectin in newly detected type 2 diabetes mellitus. Clin Endocrinol (Oxf). 2006;65(6):722–728. doi: 10.1111/j.1365-2265.2006.02658.x
  23. Li M, Xu A, Lam KSL, et al. Impact of combination therapy with amlodipine and atorvastatin on plasma adiponectin levels in hypertensive patients with coronary artery disease: combination therapy and adiponectin. Postgrad Med. 2011;123(6):66–71. doi: 10.3810/pgm.2011.11.2496
  24. Ohashi T, Shibata R, Morimoto T, et al. Correlation between circulating adiponectin levels and coronary plaque regression during aggressive lipid-lowering therapy in patients with acute coronary syndrome: subgroup analysis of JAPAN-ACS study. Atherosclerosis. 2010;212(1):237–242. doi: 10.1016/j.atherosclerosis.2010.05.005
  25. Jin H, Liu Y, Schweikert B, et al. Serial changes in exercise capacity, NT-proBNP, and adiponectin in patients with acute coronary syndrome before and after phase II rehabilitation as well as at the 12-month follow-up. Cardiol Res Pract. 2022;2022:6538296. doi: 10.1155/2022/6538296
  26. Liu Z, Liang S, Que S, et al. Meta-analysis of adiponectin as a biomarker for the detection of metabolic syndrome. Front Physiol. 2018;9:1238. doi: 10.3389/fphys.2018.01238
  27. Firova EM, Tanyanskiy DA, Shatilina LV, Denisenko AD. Svyaz’ pokazatelei obmena lipidov i uglevodov s tolerantnost’yu k fizicheskoi nagruzke u patsientov s IBS. Herald of North-Western State Medical University named after I.I. Mechnikov. 2008;(1):76–80. (In Russ.)
  28. Alberti KG, Eckel RH, Grundy SM, et al. Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Circulation. 2009;120(16):1640–1645. doi: 10.1161/CIRCULATIONAHA.109.192644
  29. Huang S, Li J, Shearer GC, et al. Longitudinal study of alcohol consumption and HDL concentrations: a community-based study. Am J Clin Nutr. 2017;105(4):905–912. doi: 10.3945/ajcn.116.144832
  30. LaMonte MJ, Eisenman PA, Adams TD, et al. Cardiorespiratory fitness and coronary heart disease risk factors: The LDS Hospital Fitness Institute Cohort. Circulation. 2000;102(14):1623–1628. doi: 10.1161/01.cir.102.14.1623
  31. Wang M, editor. Coronary artery disease: Therapeutics and drug discovery. 1st ed. 2020. Vol. 1177. doi: 10.1007/978-981-15-2517-9
  32. Ouchi N, Ohishi M, Kihara S, et al. Association of hypoadiponectinemia with impaired vasoreactivity. Hypertension. 2003;42(3): 231–234. doi: 10.1161/01.HYP.0000083488.67550.B8
  33. Kim DH, Kim C, Ding EL, et al. Adiponectin levels and the risk of hypertension: a systematic review and meta-analysis. Hypertension. 2013;62(1):27–32. doi: 10.1161/HYPERTENSIONAHA.113.01453
  34. Kshatriya S, Liu K, Salah A, et al. Obesity hypertension: the regulatory role of leptin. Int J Hypertens. 2011;2011:270624. doi: 10.4061/2011/270624
  35. Abe M, Matsuda M, Kobayashi H, et al. Effects of statins on adipose tissue inflammation: their inhibitory effect on MyD88-independent IRF3/IFN-beta pathway in macrophages. Arterioscler Thromb Vasc Biol. 2008;28(5):871–877. doi: 10.1161/ATVBAHA.107.160663
  36. He Y, Lu L, Wei X, et al. The multimerization and secretion of adiponectin are regulated by TNF-alpha. Endocrine. 2016;51(3):456–468. doi: 10.1007/s12020-015-0741-4
  37. Sahebkar A, Watts GF. Fibrate therapy and circulating adiponectin concentrations: a systematic review and meta-analysis of randomized placebo-controlled trials. Atherosclerosis. 2013;230(1):110–120. doi: 10.1016/j.atherosclerosis.2013.06.026
  38. Russell CD, Ricci MR, Brolin RE, et al. Regulation of the leptin content of obese human adipose tissue. Am J Physiol Endocrinol Metab. 2001;280(3):E399–404. doi: 10.1152/ajpendo.2001.280.3.E399
  39. Caminiti G, Volterrani M, Marazzi G, et al. Metabolic syndrome predicts lower functional recovery in female but not in male patients after an acute cardiac event. Int J Cardiol. 2009;135(3):296–301. doi: 10.1016/j.ijcard.2008.03.094
  40. Firova EM. Techenie ishemicheskoi bolezni serdtsa pri metabolicheskom sindrome [dissertation abstract]. Saint Petersburg, 2010. 21 p. (In Russ.)
  41. Ugur-Altun B, Altun A, Tatli E, et al. Relationship between insulin resistance assessed by HOMA-IR and exercise test variables in asymptomatic middle-aged patients with type 2 diabetes. J Endocrinol Invest. 2004;27:455–461. doi: 10.1007/BF03345291
  42. Ivanova EA, Myasoedova VA, Melnichenko AA, et al. Small dense low-density lipoprotein as biomarker for atherosclerotic diseases. Oxid Med Cell Longev. 2017;2017:1273042. doi: 10.1155/2017/1273042
  43. Herder C, Peltonen M, Svensson P-A, et al. Adiponectin and bariatric surgery: associations with diabetes and cardiovascular disease in the Swedish Obese Subjects Study. Diabetes Care. 2014;37(5):1401–1409. doi: 10.2337/dc13-1362

Copyright (c) 2023 Firova E.M., Tanyanskiy D.A.

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


Согласие на обработку персональных данных с помощью сервиса «Яндекс.Метрика»

1. Я (далее – «Пользователь» или «Субъект персональных данных»), осуществляя использование сайта https://journals.rcsi.science/ (далее – «Сайт»), подтверждая свою полную дееспособность даю согласие на обработку персональных данных с использованием средств автоматизации Оператору - федеральному государственному бюджетному учреждению «Российский центр научной информации» (РЦНИ), далее – «Оператор», расположенному по адресу: 119991, г. Москва, Ленинский просп., д.32А, со следующими условиями.

2. Категории обрабатываемых данных: файлы «cookies» (куки-файлы). Файлы «cookie» – это небольшой текстовый файл, который веб-сервер может хранить в браузере Пользователя. Данные файлы веб-сервер загружает на устройство Пользователя при посещении им Сайта. При каждом следующем посещении Пользователем Сайта «cookie» файлы отправляются на Сайт Оператора. Данные файлы позволяют Сайту распознавать устройство Пользователя. Содержимое такого файла может как относиться, так и не относиться к персональным данным, в зависимости от того, содержит ли такой файл персональные данные или содержит обезличенные технические данные.

3. Цель обработки персональных данных: анализ пользовательской активности с помощью сервиса «Яндекс.Метрика».

4. Категории субъектов персональных данных: все Пользователи Сайта, которые дали согласие на обработку файлов «cookie».

5. Способы обработки: сбор, запись, систематизация, накопление, хранение, уточнение (обновление, изменение), извлечение, использование, передача (доступ, предоставление), блокирование, удаление, уничтожение персональных данных.

6. Срок обработки и хранения: до получения от Субъекта персональных данных требования о прекращении обработки/отзыва согласия.

7. Способ отзыва: заявление об отзыве в письменном виде путём его направления на адрес электронной почты Оператора: info@rcsi.science или путем письменного обращения по юридическому адресу: 119991, г. Москва, Ленинский просп., д.32А

8. Субъект персональных данных вправе запретить своему оборудованию прием этих данных или ограничить прием этих данных. При отказе от получения таких данных или при ограничении приема данных некоторые функции Сайта могут работать некорректно. Субъект персональных данных обязуется сам настроить свое оборудование таким способом, чтобы оно обеспечивало адекватный его желаниям режим работы и уровень защиты данных файлов «cookie», Оператор не предоставляет технологических и правовых консультаций на темы подобного характера.

9. Порядок уничтожения персональных данных при достижении цели их обработки или при наступлении иных законных оснований определяется Оператором в соответствии с законодательством Российской Федерации.

10. Я согласен/согласна квалифицировать в качестве своей простой электронной подписи под настоящим Согласием и под Политикой обработки персональных данных выполнение мною следующего действия на сайте: https://journals.rcsi.science/ нажатие мною на интерфейсе с текстом: «Сайт использует сервис «Яндекс.Метрика» (который использует файлы «cookie») на элемент с текстом «Принять и продолжить».