Serum Adiponectin levels in Different Phenotypes of Polycystic Ovary Syndrome

Carolina Fux Otta, Paula Szafryk de Mereshian, Raquel Kaplan, Gabriel Santino Iraci, Silvia Ojeda, José Ochoa, Andrés Albrecht, Natalia Filipone, Marta Fiol de Cuneo

Cátedra de Farmacología Aplicada, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba (UNC), Córdoba, Argentina.
Cátedra de Fisiología Humana, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba (UNC), Córdoba, Argentina.
Departamento de Endocrinología y Diabetes, Hospital Universitario de Maternidad y Neonatología (HUM y N), Córdoba, Argentina.
Diangus, Diagnóstico por imágenes, docencia e investigación, Córdoba, Argentina.
Grupo de Probabilidad y Estadística, Facultad de Matemática, Astronomía y Física (UNC), Córdoba, Argentina.
Laboratorio MEGA, Rafaela, Santa Fe.

DOI: 10.4236/ojemd.2012.24019                

Abstract

Objectives: to evaluate and compare serum adiponectin levels in different phenotypes of polycystic ovary syndrome (PCOS) and to investigate their correlation with endocrine and metabolic parameters. Material and methods: we studied 5 groups of patients: A (n = 20): H (hyperandrogenism) + O (oligoanovulation) + P (polycystic ovary) [classic phenotype]; B (n = 17): H + O [classic phenotype but normal ovaries]; C (n = 15): H + P [Ovulatory phenotype]; D (n = 17): O + P [Normoandrogenic phenotype]; and E (n = 16) control group. Body mass index, waist circumference, waist/hip ratio, blood pressure and hirsutism were evaluated. Serum concentrations of adiponectin, insulin, Creactive protein, SHBG, androgens and lipids were measured. Oral glucose tolerance test was performed. Results: there were no differences between the groups in terms of age and BMI. Total cholesterol, LDL-C and triglyceride levels were higher in phenotype A than in C (P < 0.05); HDL-C was slightly lower in phenotype D compared to E (P = 0.03). HOMA-IR, insulin and glucose/insulin ratio were significantly higher in phenotypes A and D vs C and E (P < 0.05). Serum adiponectin levels were lower in phenotype A (11.6 ± 8 ug/mL) than in the rest of the groups (B: 12.5 ± 8 ug/mL; C: 20.5 ± 8 ug/mL; D: 17.4 ± 4 ug/mL; E: 20 ± 6 ug/mL). This diference reached statistical significance when comparing group A with groups C and E (P < 0.05). Adiponectin levels were significant and negatively correlated with total testosterone, free androgen index, androstenedione, DHEAS, 17-hydroxyprogesterone, LH/FSH, insulin, HOMA-IR, Creactive protein, LDL-C, triglycerides, and waist/hip ratio. A positive correlation was found with glucose/insulin ratio and HDL-C (P < 0.05). Conclusions: adiponectin serum concentrations vary according to the phenotypic expression of PCOS. Our results suggest that adiponectin could be used as a biochemical marker to identify phenotypes at increased metabolic risk.

Keywords

Polycystic Ovary Syndrome; Phenotypes; Adiponectin

Conflicts of Interest

The authors declare no conflicts of interest.

References

[1]	M. Asunción, R. M. Calvo, J. L. San Millan, J. Sancho, S. Avila and H. F. Escobar-Morreale, “A Prospective Study of the Prevalence of the Polycystic Ovary Syndrome in Unselected Caucasian Women from Spain,” The Journal of Clinical Endocrinology and Metabolism, Vol. 85, No. 7, 2000, pp. 2434-2438. doi:10.1210/jc.85.7.2434
[2]	R. Azziz, K. S. Woods, R. Reyna, T. J. Key, E. S. Knochenhauer and B. O. Vildiz, “The Prevalence and Features of the Polycystic Ovary Syndrome in Unselected Population,” The Journal of Clinical Endocrinology and Metabolism, Vol. 89, No. 6, 2004. pp. 2745-2749. doi:10.1210/jc.2003-032046
[3]	E. Diamanti-Kandarakis, C. R. Kouli, A. T. Bergiele, F. A. Filandra, T. C. Tsianateli, G. G. Spina, E. D. Zapanti and M. I. Bartzis, “A Survey of the Polycystic Ovary Syndrome in the Greek Island of Lesbos: Hormonal and Metabolic Profile,” The Journal of Clinical Endocrinology and Metabolism, Vol. 84, No. 11, 1999, pp. 4006-4011. doi:10.1210/jc.84.11.4006
[4]	M. O. Goodarzi, D. A. Dumesic, G. Chazenbalk and R. Azziz, “Polycystic Ovary Syndrome: Etiology, Pathogenesis and Diagnosis,” Nature Reviews. Endocrinology, Vol. 7, No. 4, 2011, pp. 219-231. doi:10.1038/nrendo.2010.217
[5]	Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group, “Revised 2003 Consensus on Diagnostic Criteria and Long-Term Health Risks Related to PCOS,” Fertility and Sterility, Vol. 81, No. 1, 2004, pp. 19-25. doi:10.1016/j.fertnstert.2003.10.004
[6]	J. K. Zawadzki and A. Dunaif, “Diagnostic Criteria for Polycystic Ovary Syndrome: Towards a Rational Approach,” In: A. Dunaif, J. R. Givens, F. Haseltine and G. R. Merriam, Eds., Polycystic Ovary Syndrome, Blackwell Scientific, Boston, 1992, pp. 377-384.
[7]	S. Franks, “Diagnosis of Polycystic Ovary Syndrome: In Defense of the Rotterdam Criteria,” The Journal of Clinical Endocrinology and Metabolism, Vol. 91, No. 3, 2006, pp. 786-789. doi:10.1210/jc.2005-2501
[8]	R. Azziz, “Diagnosis of Polycystic Ovary Syndrome: The Rotterdam Criteria Are Premature,” The Journal of Clinical Endocrinology and Metabolism, Vol. 91, No. 3, 2006, pp. 781-785. doi:10.1210/jc.2005-2153
[9]	L. Moran and H. Teede, “Metabolic Features of the Reproductive Phenotypes of Polycystic Ovary Syndrome,” Human Reproduction Update, Vol. 15, No. 4, 2009, pp. 477-488. doi:10.1093/humupd/dmp008
[10]	A. Dunaif, “Insulin Resistance and the Polycystic Ovary Syndrome: Mechanism and Implications for Pathogenesis,” Endocrine Reviews, Vol. 18, No. 6, 1997, pp. 774-800. doi:10.1210/er.18.6.774
[11]	R. A. Wild, E. Carmina, E. Diamanti-Kandarakis, A. Dokras, H. F. Escobar-Morreale, W. Futterweit, R. Lobo, R. J. Norman, D. A. Talbott and E. Dumesic, “Assessment of Cardiovascular Risk and Prevention of Cardiovascular Disease in Women with the Polycystic Ovary Syndrome: A Consensus Statement by the Androgen Excess and Polycystic Ovary Syndrome (AE-PCOS) Society,” The Journal of Clinical Endocrinology and Metabolism, Vol. 95, No. 5, 2010, pp. 2038-2049. doi:10.1210/jc.2009-2724
[12]	T. Kadowaki and T. Yamauchi, “Adiponectin and Adiponectin Receptors,” Endocrine Reviews, Vol. 26, No. 3, 2005, pp. 439-451. doi:10.1210/er.2005-0005
[13]	H. F. Escobar-Morreale and J San Millán, “Abdominal Adiposity and the Polycystic Ovary Syndrome,” Trends in Endocrinology and Metabolism, Vol. 18, No. 7, 2007, pp. 266-272. doi:10.1016/j.tem.2007.07.003
[14]	G. J. Hausman and C. R. Barb, “Adipose Tissue and the Reproductive Axis: Biological Aspects,” Endocrine Development, Vol. 19, 2010, pp. 31-44. doi:10.1159/000316895
[15]	L. Manner?s-Holm, H. Leonhardt, J. Kullberg, E. Jennische, A. Odén, G. Holm, M. Hellstr?m, L. L?nn, G. Olivecrona, E. Stener-Victorin and M. L?nn, “Adipose Tissue Has Aberrant Morphology and Function in PCOS: Enlarged Adipocytes and Low Serum Adiponectin, but Not Circulating Sex Steroids, Are Strongly Associated with Insulin Resistance,” The Journal of Clinical Endocrinology and Metabolism, Vol. 96, No. 2, 2011, pp. 304-311. doi:10.1210/jc.2010-1290
[16]	R. Hatch, R. L. Rosenfield, M. H. Kim and D. Tredway, “Hirsutism: Implications, Etiology, and Management,” American Journal of Obstetrics and Gynecology, Vol. 40, No. 7, 1981, pp. 815-830.
[17]	J. E. Morley, P. Patrick and H. M. Perry, “3rd Evaluation of Assays Available to Measure Free Testosterone,” Metabolism, Vol. 51, No. 5, 2002, pp. 554-559. doi:10.1053/meta.2002.31975
[18]	D. R. Matthews, J. P. Hosker, A. S. Rudenski, B. A. Naylor, D. F. Treacher and R. C. Turner, “Homeostasis Model Assessment: Insulin Resistance and Beta-Cell Function from Fasting Plasma Glucose and Insulin Concentrations in Man,” Diabetologia, Vol. 28, No. 7, 1985, pp. 412-419. doi:10.1007/BF00280883
[19]	H. F. Escobar-Morreale, G. Villuendas, J. I. Botella-Carretero, F. Alvarez-Blasco, R. Sanchón, M. LuqueRamírez and J. L. San Millán, “Adiponectin and Resistin in PCOS: A Clinical, Biochemical and Molecular Genetic Study,” Human Reproduction, Vol. 21, No. 9, 2006, pp. 2257-2265. doi:10.1093/humrep/del146
[20]	M. Yilmaz, N. Bukan, H. Demirci, C. Oztürk, E. Kan, G. Ayvaz and M. Arslan, “Serum Resistin and Adiponectin Levels in Women with Polycystic Ovary Syndrome,” Gynecological Endocrinology, Vol. 25, No. 4, 2009, 246-252. doi:10.1080/09513590802653833
[21]	A. Xu, K. W. Chan, R. L. Hoo, Y. Wang, K. C. Tan, J. Zhang, B. Chen, M. C. Lam, C. Tse, G. J. Cooper and K. S. Lam, “Testosterone Selectively Reduces the High Molecular Weight Form of Adiponectin by Inhibiting Its Secretion from Adipocytes,” Journal of Biological Chemistry, Vol. 280, No. 18, 2005, pp. 18073-18080. doi:10.1074/jbc.M414231200
[22]	A. Karkanaki, A. Piouka, I. Katsilis, D. Farmakiotis, D. Mecut and D. Panidis, “Adiponectin Levels Reflect the Different Phenotypes of Polycystic Ovary Syndrome: Study in Normal Weight, Normoinsulinemic Patients,” Fertility and Sterility, Vol. 92, No. 6, 2009, pp. 2078-2081. doi:10.1016/j.fertnstert.2009.06.034
[23]	L. Sieminska, B. Marek, B. Kos-Kudla, D. Niedziolka, D. Kajdaniuk, M. Nowak and J. Glogowska-Szelag, “Serum Adiponectin in Women with Polycystic Ovarian Syndrome and Its Relation to Clinical, Metabolic and Endocrine Parameters,” Journal of Endocrinological Investigation, Vol. 27, No. 6, 2004, pp. 528-534.
[24]	J. M. Elbers, E. J. Giltay, T. Teerlink, P. G. Scheffer, H. Asscheman, J. C. Seidell and L. J. Gooren, “Effects of Sex Steroids on Components of the Insulin Resistance Syndrome in Transsexual Subjects,” Clinical Endocrinology, Vol. 58, No. 5, 2003, pp. 562-571. doi:10.1046/j.1365-2265.2003.01753.x
[25]	A. Gambineri, L. Patton, A. Vaccina, M. Cacciari, A. M. Morselli-Labate, C. Cavazza, U. Pagotto and R. Pasquali, “Treatment with Flutamide, Metformin, and Their Combination Added to a Hypocaloric Diet in Overweight-Obese Women with Polycystic Ovary Syndrome: A Randomized, 12-Month, Placebo-Controlled Study,” The Journal of Clinical Endocrinology and Metabolism, Vol. 91, No. 10, 2006, pp. 3970-3980. doi:10.1210/jc.2005-2250
[26]	T. M. Barber, M. Hazell, C. Christodoulides, S. J. Golding, C. Alvey, K. Burling, A. Vidal-Puig, N. P. Groome, J. A. Wass, S. Franks and M. I. McCarthy, “Serum Levels of Retinol-Binding Protein 4 and Adiponectin in Women with Polycystic Ovary Syndrome: Associations with Visceral Fat but No Evidence for Fat Mass-Independent Effects on Pathogenesis in This Condition,” The Journal of Clinical Endocrinology and Metabolism, Vol. 93, No. 7, 2008, pp. 2859-2865. doi:10.1210/jc.2007-2759
[27]	E. Carmina, S. Bucchieri, P. Mansueto, G. Rini, M. Ferin and R. A. Lobo, “Circulating Levels of Adipose Products and Differences in Fat Distribution in the Ovulatory and Anovulatory Phenotypes of Polycystic Ovary Syndrome,” Fertility and Sterility, Vol. 91, No. 4, 2009, pp. 1332-1335. doi:10.1016/j.fertnstert.2008.03.007
[28]	L. Xian, W. He, F. Pang and Y. Hu, “ADIPOQ Gene Polymorphisms and Susceptibility to Polycystic Ovary Syndrome: A HuGE Survey and Meta-Analysis,” European Journal of Obstetrics Gynecology and Reproductive Biology, Vol. 161, No. 2, 2012, pp. 117-124. doi:10.1016/j.ejogrb.2011.12.017