Özgür YILMAZ, Halil Gürsoy PALA, Burcu Artunç ÜLKÜMEN

Polikistik Over Sendromlu ve Normal Menstrüel Sikluslu Kadınlarda İnsülin Duyarlılığı Düzeylerinin Kıyaslanması

Amaç: Polikistik over sendromu (PKOS)’un patofizyolojisi tam olarak anlaşılamamıştır. Bununla beraber insülin direncinin sendromun gelişmesinde merkezi bir rolü olduğu düşünülmektedir. Bu çalışmada insülin duyarlılığı durumunu yansıtan non-invaziv kantitatif insülin duyarlılığı hesaplama indeksi’ nin (quantitative insulin sensitivity check index-QUICKI) değerlerini PKOS’u olan ve adet düzeni normal olan kadınlar arasında karşılaştırıldı. Ayrıca bu indeksin klinik pratikte PKOS daki insülin duyarlığı/direnci durumundaki kullanılabilirliğinin incelenmesi amaçlandı. Materyal ve Metot: Retrospektif olarak 50 PKOS’lu kadın ile adet düzeni normal olan, 50 sağlıklı kadın yaş ve vücut kitle indeksi kıyaslamalı incelendi. Serum açlık glukoz, insulin ve testosteron konsantrasyonları değerlendirildi. QUICKI ve insulin direncinin homeostasis model değerlendirmesi (homeostasis model assessment of insulin resistance-HOMA-IR) indeksleri hesaplandı. Bulgular: Her iki grup arasında QUICKI (PKOS grubu=0,329±0,022 ve kontrol grubu=0,333±0,019; p=0,39) ve HOMA-IR (PKOS grubu= 3,057±1,468 ve kontrol grubu=2,717±1,037; p=0,184) yönünden anlamlı fark bulunmadı. QUICKI ile serum açlık glukoz konsantrasyonları (p=0,136) ve serum testosteron konsantrasyonları (p=0. 227), arasında anlamlı korelasyon saptanmaz iken; hem serum açlık insülin konsantrasyonları (r=-0,925, p<0,001), hem de HOMA-IR (r=-0,95, p<0,001), arasında anlamlı negatif korelasyon saptandı. Sonuç: PKOS’lu kadınlarda insülin duyarlılığı değerlendirilmesi gereken bir klinik durumdur. PKOS’da ülkemize ait insülin duyarlılığı/ direnci durumlarını yansıtan güvenilir eşik değerleri halen mevcut değildir. Bundan ötürü ilerideki çalışmaların PKOS’daki insulin duyarlılığını prospektif olarak ortaya koyması önerilmektedir.

Anahtar Kelimeler:

PKOS, QUICKI, insulin duyarlılığı

Comparison of Insulin Sensitivity Levels in Women with PCOS and Women with Regular Menses

Aim: Although pathophysiology of polycystic ovary syndrome (PCOS) has not been fully understood, it has been suggested that decreasing insulin sensitivity may have a pivotal role in this disorder. In this study it was aimed that as a non invasive technique, quantitative insulin sensitivity check index-(QUICKI) levels which has reflected the insulin sensitivity status, were compared in women with PCOS and regular menses. Additionally, we evaluated whether this index may have been used in clinical practice of PCOS. Material and Method: Fifty women with PCOS and fifty age and body mass index matched healthy women with regular menses were retrospectively evaluated. Serum fasting glucose, insulin and testosterone concentrations were assessed. QUICKI and homeostasis model assessment of insulin resistance (HOMA-IR) indice was calculated. Results: There were no significant differences in between two groups according to both QUICKI (PCOS group=0.329±0.022 vs. Control group=0.333±0.019; p=0.39) and HOMA-IR (PCOS group=3.057±1.468 vs. Control group=2.717±1.037; p=0.184). QUICKI was not significantly correlated with glucose (p=0.136) and testosterone levels (p=0.227), whereas significantly negative correlated with both insulin (r=-0.925, p<0.001), and HOMA-IR (r=-0.95, p<0.001). Conclusion: Insulin sensitivity which should be appreciated a clinical condition in women with PCOS. In our country reliable reference ranges of insulin sensitivity/resistance status in PCOS still have not avaible. Therefore, it was suggested that advanced studies should prospectively execute the cut of values of insulin sensitivity in PCOS.

Keywords:

PCOS, QUICKI, insulin sensitivity,

PDF

___

1. Azziz R, Woods KS, Reyna R, Key TJ, Knochenhauer ES,Yildiz BO. The prevalence and features of the polycystic ovary syndrome in an unselected population. J Clin Endocrinol Metab2004;89:2745–9.
2. Dunaif A, Segal KR, Futterweit W, Dobrjansky A. Profoundperipheral insulin resistance, independent of obesity, in polycystic ovary syndrome. Diabetes 1989;38:1165–74.
3. Shi Y, Cui Y, Sun X, Ma G, Ma Z, Gao Q, et al. Hypertension in women with polycystic ovary syndrome: prevalence and associated cardiovascular risk factors. Eur J Obstet Gynecol Reprod Biol 2014;173:66–70.
4. Cheung LP, Ma RC, Lam PM, Lok IH, Haines CJ, So WY, et al. Cardiovascular risks and metabolic syndrome in Hong Kong Chinese women with polycystic ovary syndrome. Hum Reprod 2008;23:1431–8.
5. Hong Y, Zhao XM, Huang LL, Li L, Chen XL, Yang DZ. Serum visfatin is elevated in Chinese women with polycystic ovary syndrome, but might not be a reliable predictor of their glucose intolerance. J Biol Regul Homeost Agents 2012;26:221–9.
6. Kubota T. Update in polycystic ovary syndrome: new criteria of diagnosis and treatment in Japan. Reprod Med Biol 2013;12:71–7. 7. Legro RS, Arslanian SA, Ehrmann DA, Hoeger KM, Murad MH, Pasquali R, et al. Endocrine Society. Diagnosis and treatment of polycystic ovary syndrome: an endocrine society clinical practice guideline. J Clin Endocrinol Metab 2013;12:4565–92.
8. Katz A, Nambi SS, Mather K, Baron AD, Follmann DA, Sullivan G, et al. Quantitative insulin sensitivity check index: a simple, accurate method for assessing insulin sensitivity in humans. J Clin Endocrinol Metab 2000;85:2402–10.
9. Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetol 1985;28:412–19.
10. Mohan BS. Mathematical indices of insulin resistance and body mass index in polycystic ovarian syndrome. J Obstet Gynecol India 2005;55:159–62.
11. Wild S, Pierpoint T, McKeigue P, Jacobs H. Cardiovascular disease in women with polycystic ovary syndrome at long-term follow-up: a retrospective cohort study. Clin Endocrinol (Oxf ) 2000;52:595– 600.
12. Li W, Li Q. Dysregulation of glucose metabolism even in Chinese PCOS women with normal glucose tolerance. Endocrinol J 2012;59:765–70.
13. Stovall DW, Bailey AP, Pastore LM. Assessment of insulin resistance and impaired glucose tolerance in lean women with polycystic ovary syndrome. J Womens Health (Larchmt) 2011;20:37–43.
14. Salley KE, Wickham EP, Cheang KI, Essah PA, Karjane NW, Nestler JE. Glucose intolerance in polycystic ovary syndrome- -a position statement of the Androgen Excess Society. J Clin Endocrinol Metab 2007;92:4546–56.
15. Legro R, Finegood D, Dunaif A. A fasting glucose to insulin ratio is a useful measure of insulin sensitivity in women with polycystic ovary syndrome. J Clin Endocrinol Metab 1998;83:2694–98.
16. Laakso M. How good a marker is insulin level for insulin resistance? Am J Epidemiol 1993;137:959–65.
17. Kauffman RP, Baker VM, Dimarino P, Gimpel T, Castracane VD. Polycystic ovarian syndrome and insulin resistance in white and Mexican American women: A comparison of two distinct populations. Am J Obstet Gynecol 2002;187:1362–9.
18. Chang RJ, Nakamura RM, Judd HL, Kaplan SA. Insulin resistance in nonobese patients with polycystic ovarian disease. J Clin Endocrinol Metab 1983;57:356–9. 19. Holte J. Polycystic ovary syndrome and insulin resistance: thrifty genes struggling with over-feeding and sedentary life style? J Endocrinol Invest 1998;21:589–601.
20. Cupisti S, Häberle L, Dittrich R, Oppelt PG, Reissmann C, Kronawitter D, et al. Smoking is associated with increased free testosterone and fasting insulin levels in women with polycystic ovary syndrome, resulting in aggravated insulin resistance. Fertil Steril 2010;94:673–7.
21. Penaforte FR, Japur CC, Diez-Garcia RW, Chiarello PG. Upper trunk fat assessment and its relationship with metabolic and biochemical variables and body fat in polycystic ovary syndrome. J Hum Nutr Diet 2011;24:39–46.
22. Takeuchi T, Tsutsumi O, Taketani Y. Abnormal response of insulin to glucose loading and assessment of insulin resistance in non-obese patients with polycystic ovary syndrome. Gynecol Endocrinol 2008;24:385–91.