Central European Journal of Medicine

, Volume 8, Issue 5, pp 679–684 | Cite as

MCP-1 and fetuin A levels in patients with PCOS and/or obesity before and after metformin treatment

  • Antoaneta Gateva
  • Zdravko Kamenov
  • Adelina Tsakova
Research Article



The aim of the study was to investigate MCP-1 and fetuin A levels in women with PCOS and/or obesity before and after metformin treatment.


In the study consisted of 59 patients. Anthropometric measurements and biochemical tests, including MCP-1 and fetuin A measurement, were performed. For patients that were diagnosed with insulin resistance and started metformin treatment all the laboratory tests and anthropometric measurements were repeated after 6 months.


MCP-1 and fetuin A levels did not differ between patients with obesity with and without PCOS, between patients with PCOS with and without obesity, insulin resistance, arterial hypertension, dyslipidemia or menstrual disturbances. MCP-1 levels were significantly higher in patients with hyperandrogenemia than in patients without (456.3±141.1pmol/L vs. 372.5±108.5 pmol/L), while fetuin A levels were significantly higher in patients with metabolic syndrome (MetS) than in patients without MetS (278.5±41.1 mcg/ml vs. 240.0±42.0 mcg/ml). There was no significant change in MCP-1 and fetuin A levels after of metformin treatment.


MCP- 1 levels are higher in patients with hyperandrogenemia and fetiun A levels are higher in patients with metabolic syndrome. MCP-1 and fetuin A levels do not change significantly after metformin treatment.


Atherosclerosis Cardiovascular risk Metabolic syndrome 


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  1. [1]
    Ehrmann, D.A., et al., Prevalence of impaired glucose tolerance and diabetes in women with polycystic ovary syndrome. Diabetes Care, 1999. 22(1): p. 141–146PubMedCrossRefGoogle Scholar
  2. [2]
    Legro, R.S., et al., Prevalence and predictors of risk for type 2 diabetes mellitus and impaired glucose tolerance in polycystic ovary syndrome: a prospective, controlled study in 254 affected women. J Clin Endocrinol Metab, 1999. 84(1): p. 165–169PubMedCrossRefGoogle Scholar
  3. [3]
    Bjorntorp, P., The android woman—a risky condition. J Intern Med, 1996. 239(2): p. 105–110PubMedCrossRefGoogle Scholar
  4. [4]
    Vrbikova, J., et al., Cardiovascular risk factors in young Czech females with polycystic ovary syndrome. Hum Reprod, 2003. 18(5): p. 980–984PubMedCrossRefGoogle Scholar
  5. [5]
    Talbott, E., et al., Coronary heart disease risk factors in women with polycystic ovary syndrome. Arterioscler Thromb Vasc Biol, 1995. 15(7): p. 821–826PubMedCrossRefGoogle Scholar
  6. [6]
    Talbott, E., et al., Adverse lipid and coronary heart disease risk profiles in young women with polycystic ovary syndrome: results of a case-control study. J Clin Epidemiol, 1998. 51(5): p. 415–422PubMedCrossRefGoogle Scholar
  7. [7]
    Wild, R.A., P. Alaupovic, and I.J. Parker, Lipid and apolipoprotein abnormalities in hirsute women. I. The association with insulin resistance. Am J Obstet Gynecol, 1992. 166(4): p. 1191–1196; discussion 1196–1997PubMedCrossRefGoogle Scholar
  8. [8]
    Paradisi, G., et al., Polycystic ovary syndrome is associated with endothelial dysfunction. Circulation, 2001. 103(10): p. 1410–1415PubMedCrossRefGoogle Scholar
  9. [9]
    Lakhani, K., et al., Internal carotid-artery response to 5% carbon dioxide in women with polycystic ovaries. Lancet, 2000. 356(9236): p. 1166–1167PubMedCrossRefGoogle Scholar
  10. [10]
    Davila-Roman, V.G., et al., Altered myocardial fatty acid and glucose metabolism in idiopathic dilated cardiomyopathy. J Am Coll Cardiol, 2002. 40(2): p. 271–277PubMedCrossRefGoogle Scholar
  11. [11]
    Gerszten, R.E., et al., Chemokines, leukocytes, and atherosclerosis. J Lab Clin Med, 2000. 136(2): p. 87–92PubMedCrossRefGoogle Scholar
  12. [12]
    Aiello, R.J., et al., Monocyte chemoattractant protein- 1 accelerates atherosclerosis in apolipoprotein E-deficient mice. Arterioscler Thromb Vasc Biol, 1999. 19(6): p. 1518–1525PubMedCrossRefGoogle Scholar
  13. [13]
    Gu, L., et al., Absence of monocyte chemoattractant protein-1 reduces atherosclerosis in low density lipoprotein receptor-deficient mice. Mol Cell, 1998. 2(2): p. 275–281PubMedCrossRefGoogle Scholar
  14. [14]
    Sartipy, P. and D.J. Loskutoff, Monocyte chemoattractant protein 1 in obesity and insulin resistance. Proc Natl Acad Sci USA, 2003. 100(12): p. 7265–7270PubMedCrossRefGoogle Scholar
  15. [15]
    Hu, W.H., et al., [Monocyte chemoattractant protein- 1 and its correlation with lipoprotein in polycystic ovary syndrome]. Beijing Da Xue Xue Bao, 2006. 38(5): p. 487–491PubMedGoogle Scholar
  16. [16]
    Gonzalez, F., et al., Evidence of proatherogenic inflammation in polycystic ovary syndrome. Metabolism, 2009. 58(7): p. 954–962PubMedCrossRefGoogle Scholar
  17. [17]
    Glintborg, D., et al., Plasma monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-1alpha are increased in patients with polycystic ovary syndrome (PCOS) and associated with adiposity, but unaffected by pioglitazone treatment. Clin Endocrinol (Oxf), 2009. 71(5): p. 652–658CrossRefGoogle Scholar
  18. [18]
    Auberger, P., et al., Characterization of a natural inhibitor of the insulin receptor tyrosine kinase: cDNA cloning, purification, and anti-mitogenic activity. Cell, 1989. 58(4): p. 631–640PubMedCrossRefGoogle Scholar
  19. [19]
    Rauth, G., et al., The nucleotide and partial amino acid sequences of rat fetuin. Identity with the natural tyrosine kinase inhibitor of the rat insulin receptor. Eur J Biochem, 1992. 204(2): p. 523–529PubMedCrossRefGoogle Scholar
  20. [20]
    Srinivas, P.R., et al., Serum alpha 2-HSglycoprotein is an inhibitor of the human insulin receptor at the tyrosine kinase level. Mol Endocrinol, 1993. 7(11): p. 1445–1455PubMedCrossRefGoogle Scholar
  21. [21]
    Mathews, S.T., et al., Bovine fetuin is an inhibitor of insulin receptor tyrosine kinase. Life Sci, 1997. 61(16): p. 1583–1592PubMedCrossRefGoogle Scholar
  22. [22]
    Stefan, N., et al., Alpha2-Heremans-Schmid glycoprotein/fetuin-A is associated with insulin resistance and fat accumulation in the liver in humans. Diabetes Care, 2006. 29(4): p. 853–857PubMedCrossRefGoogle Scholar
  23. [23]
    Mori, K., et al., Association of serum fetuin-A with insulin resistance in type 2 diabetic and nondiabetic subjects. Diabetes Care, 2006. 29(2): p. 468PubMedCrossRefGoogle Scholar
  24. [24]
    Hennige, A.M., et al., Fetuin-A induces cytokine expression and suppresses adiponectin production. PLoS One, 2008. 3(3): p. e1765PubMedCrossRefGoogle Scholar
  25. [25]
    Stefan, N., et al., Plasma fetuin-A levels and the risk of type 2 diabetes. Diabetes, 2008. 57(10): p. 2762–2767PubMedCrossRefGoogle Scholar
  26. [26]
    Roos, M., et al., Fetuin-A and arterial stiffness in patients with normal kidney function. Regul Pept, 2009. 154(1–3): p. 39–43PubMedCrossRefGoogle Scholar
  27. [27]
    Ix, J.H., et al., Association between human fetuin-A and the metabolic syndrome: data from the Heart and Soul Study. Circulation, 2006. 113(14): p. 1760–1767PubMedCrossRefGoogle Scholar
  28. [28]
    Weikert, C., et al., Plasma fetuin-a levels and the risk of myocardial infarction and ischemic stroke. Circulation, 2008. 118(24): p. 2555–2562PubMedCrossRefGoogle Scholar
  29. [29]
    Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome (PCOS). Hum Reprod, 2004. 19(1): p. 41–47Google Scholar
  30. [30]
    Physical status: the use and interpretation of anthropometry. Report of a WHO Expert Committee. World Health Organ Tech Rep Ser, 1995. 854: p. 1–452Google Scholar
  31. [31]
    Hu, W.H., J. Qiao, and M.Z. Li, [Association of monocyte chemoattractant protein-1 and the clinical characteristics of polycystic ovary syndrome: analysis of 65 cases]. Zhonghua Yi Xue Za Zhi, 2007. 87(11): p. 721–724PubMedGoogle Scholar
  32. [32]
    Lindholm, A., et al., No difference in markers of adipose tissue inflammation between overweight women with polycystic ovary syndrome and weight-matched controls. Hum Reprod, 2011. 26(6): p. 1478–1485PubMedCrossRefGoogle Scholar
  33. [33]
    Zhu, J.P., et al., [Role of testosterone in tumor necrosis factor-alpha and monocyte chemotactic protein- 1 expression in mouse macrophage RAW264.7 and its molecular mechanism]. Zhonghua Yi Xue Za Zhi, 2009. 89(35): p. 2500–2503PubMedGoogle Scholar
  34. [34]
    Ishibashi, A., et al., Serum fetuin-A is an independent marker of insulin resistance in Japanese men. J Atheroscler Thromb, 2010. 17(9): p. 925–933PubMedCrossRefGoogle Scholar
  35. [35]
    Reinehr, T. and C.L. Roth, Fetuin-A and its relation to metabolic syndrome and fatty liver disease in obese children before and after weight loss. J Clin Endocrinol Metab, 2008. 93(11): p. 4479–4485PubMedCrossRefGoogle Scholar
  36. [36]
    Xu, Y., et al., Serum fetuin-A is correlated with metabolic syndrome in middle-aged and elderly Chinese. Atherosclerosis, 2011. 216(1): p. 180–186PubMedCrossRefGoogle Scholar
  37. [37]
    Mori, K., et al., Effects of pioglitazone on serum fetuin-A levels in patients with type 2 diabetes mellitus. Metabolism, 2008. 57(9): p. 1248–1252PubMedCrossRefGoogle Scholar

Copyright information

© Versita Warsaw and Springer-Verlag Berlin Heidelberg 2013

Authors and Affiliations

  • Antoaneta Gateva
    • 1
  • Zdravko Kamenov
    • 1
  • Adelina Tsakova
    • 2
  1. 1.Clinic of EndocrinologyUniversity Hospital Alexandrovska, Medical UniversitySofiaBulgaria
  2. 2.Central clinical laboratoryUniversity Hospital Alexandrovska, Medical UniversitySofiaBulgaria

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