Polikistik over sendromunda insülin rezistansı ve nöropeptid Y düzeyleri arasındaki ilişkinin araştırılması

Abstract

Amaç: Çalışmanın amacı, polikistik over sendromu (PKOS)

patogenezinde önemli yeri olan nöropeptid Y (NPY) ve insülin

direnci arasındaki ilişkinin araştırılmasıdır.

Gereçler ve Yöntemler: Bu çalışma Mayıs 2012 ve Mayıs 2013

tarihleri arasında yapılmıştır. Çalışmaya doğurganlık çağındaki 45

PKOS hastası ve 44 sağlıklı kontrol grubu dahil edilmiştir. PKOS

grubuna erken foliküler fazda insulin, açlık kan şekeri, folikül

stimüle edici hormon (FSH), luteize edici hormon (LH), prolaktin,

testesteron, dehidroepiandrosteron sülfat (DHEA-S), tiroid

stimüle edici hormon (TSH), kortizol, östrodiol ve NPY düzeyleri

bakılırken, kontrol grubuna insülin, açlık kan şekeri, prolaktin,

DHEA-S, TSH, kortizol, 17-OH progesteron düzeyleri incelendi.

Homeostatik model insulin direnci değerlendirme (HOMA-IR)

testi skorları hesaplandı ve antropometrik ölçümler kaydedildi.

Pelvik ultrasonografi yapıldı.

Bulgular: İnsulin direncini gösteren açlık kan insülin düzeyi

ve HOMA-IR skoru, obez PKOS grubunda normal kilolu PKOS

ve kontrol grubuna göre yüksek bulundu. NPY düzeyleri obezyüksek

kilolu PKOS grubunda normal kilolu PKOS ve kontrol

grubuna göre yüksek bulundu ancak istatistiksel olarak anlamlı

değildi (P>0,05). NPY düzeyleri insülin rezistansı olan ve olmayan

hastalar arasında değişiklik göstermedi.

Sonuç: İnsülin rezistansı ve NPY düzeyleri arasında

korelasyon saptanmadı ancak NPY düzeyleri, kilolu PCOS

hastalarında yüksekti.

Keywords

• Polikistik over sendromu,İnsülin rezistansı,Nöropeptid Y

Investigation of the relationship between insulin resistance and neuropeptide Y levels in polycystic ovary syndrome

Abstract

Objective: The aim of study is to investigate the relationship between neuropeptide Y (NPY) and insulin resistance which is important in the pathogenesis of poliycstic ovary syndrome (PCOS). Material and Methods: This study was conducted between May 2012 and May 2013. The study included 45 patients with PCOS and 44 healthy controls at productive age. Insulin, fasting blood sugar, follicle-stimulating hormone (FSH), luteinizing hormone (LH), prolactine, testestorone, dehydroepiandrosterone sulfate (DHEA-S), thyroid stimulating hormone (TSH), cortisole, estradiol, NPY levels were measured at early follicular phase in patients with PCOS while insulin, fasting blood sugar, prolactine, DHEA-S, TSH, cortisole, 17-OH progesterone levels were measured in control group. Homeostatic model assessment for insulin resistance (HOMA-IR) scores were calculated and antrepometric measures recorded. Pelvic ultrasonography was performed. Results: Fasting insulin levels and HOMA-IR scores showed insulin resistance to be higher in obese patients with PCOS than healthy control subjects and patients with normal weight PCOS. NPY levels found to be higher in obese-overweight patients with PCOS than healthy control subjects and patients with normal weight but it was not statistically significant (P>0.05). NPY levels did not differ in patients with and without insulin resistance. Conclusion: No correlation dedected between insülin resistance and NPY levels but NPY levels were high in overweight PCOS patients.

Keywords

• Poliycstic ovary syndrome,Insulin resistance,Neuropeptide Y

References

1. 1. Ehrmann DA. Polycystic ovary syndrome. N Engl J Med 2005;352:1223-36. doi:10.1056/NEJM200.506.303522620
2. 2. Tsilchorozidou T, Overton C, Conway GS. The pathophysiology of polycystic ovary syndrome. Clin Endocrinol Rev 2004; 60:1-17. doi:10.1046/j.1365- 2265.2003.01842.x
3. 3. Kayaalp O. Tıbbi Farmakoloji. Cilt:2 9. Baskı. Ankara: Hacettepe Taş Kitabevi, 2000.
4. 4. Herzog, H. Neuropeptide Y and energy homeostasis: insights from Y receptor knockout models. Eur J Pharmacol 2003; 48:21-9. doi:10.1016/j.ejphar.2003.08.089
5. 5. Azziz R, Carmina E, Dewailly D, et al. The Androgen Excess and PCOS Society criteria for the polycystic ovary syndrome: the complete task force report. Fertil Steril 2009;91:456-88. doi: 10.1016/j.fertnstert.2008.06.035.
6. 6. The Rotterdam ESHRE/ASRM-Sponsered PCOS Workshop Group. Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome. Fertil Steril 2004; 81:19-25. doi:10.1016/j. fertnstert.2003.10.004
7. 7. Bayram F, Ünlühızarcı K, Kelestimur F. Potential utility of insulin sensitizers in the treatment of polycystic ovary syndrome. Treat Endocrinol 2002;1:45-53. doi:10.2165/00024.677.200201010-00005
8. 8. Dunaif A. Insulin resistance and the polycystic ovary syndrome: mechanism and implications for pathogenesis. Endocr Rev 1997;18:774-800. doi:10.1210/ edrv.18.6.0318

9. 9. Barbieri RL, Ryan KJ. Hyperandrogenism, insulin resistance, and acanthosis nigricans syndrome: a common endocrinopathy with distinct pathophysiologic features. Am J Obstet Gynecol 1983; 147: 90-101. doi:10.1016/0002- 9378(83)90091-1
10. 10. Poretsky L, Kalin MF. The gonadotropic function of insulin. Endocr Rev 1987; 8:132-41. doi:10.1210/edrv-8-2-132
11. 11. Poretsky L. On the paradox of insulin-induced hyperandrogenism in insulin-resistant states. Endocr Rev 1991; 12:3-13. doi:10.1210/edrv-12-1-3
12. 12. Tsilchorozidou T, Overton C, Convay SG. The Pathophysiology of polycystic ovary syndrome. Clin Endocrinol 2004; 60:1- 28. doi:10.1046/j.1365-2265.2003.01842.x
13. 13. Dunaif A, Segal KR, Futterweit W, Dobrjansky A. Profound peripheral insulin resistance, independent of obesity in polycystic ovary syndrome. Diabetes 1989;38:1165-74. doi:10.2337/diab.38.9.1165
14. 14. Dunaif A, Segal KR, Shelley DR, et al. Evidence for dinstinctive and intrinsic defect in insulin action in polycystic ovary syndrome. Diabetes 1992;41:1257-66. doi:10.2337/diab.41.10.1257
15. 15. Dunaif A, Kandarakis DE. New perspectives in polycystic ovary syndrome. Trends Endocrinol Metab 1996;7: 267-71. doi:10.1016/S1043-2760(96)00125-7
16. 16. Carmina E, Koyama T, Chang L, et al. Does ethnicity influence the prevalence of adrenal hyperandrogenism and insulin resistance in polycystic ovary syndrome? Am J Obstet Gynecol 1992; 167:1807-12. doi:10.1016/0002- 9378(92)91779-A
17. 17. Dale PO, Tanbo T, Vaaler S, Abyholm T. Body weight, hyperinsulinemia and gonadotropin levels in the polycystic ovarian syndrome: evidence of two distinct populations. Fertil Steril 1992; 58: 487-91. doi:10.1016/S0015- 0282(16)55249-2
18. 18. Bonora E, Targher G, Alberiche M, et al. Homeostasis model assessment closely mirrors the glucose clamp technique in the assessment of insulin sensitivity: studies in subjects with various degrees of glucose tolerance and insulin sensitivity. Diabetes Care 2000;23:57-63. doi:10.2337/diacare.23.1.57
19. 19. Herbert CM, Hill GA, Diamond MP. The use of the intravenous glucose tolerans test to evaluate nonobese hyperandrogenemic women. Fertil Steril 1990;53: 647-53. doi:10.1016/S0015-0282(16)53458-X
20. 20. Ciaraldi TP, el-Roeiy A, Madar Z, Reichart D, Olefsky JM, Yen SS. Cellular mechanisms of insulin resistance in polycystic ovary syndrome. J Clin Endocrinol Metab 1992;75: 557-83. doi:10.1210/jcem.75.2.1322430
21. 21. Barber TM, McCarthy M, Wass JA, Franks S. Obesity and polycystic ovary syndrome. Clinic Endocrinol 2006; 65:135- 45. doi:10.1111/j.1365-2265.2006.02587.x
22. 22. Franks S. Polycystic ovary syndrome. N Eng J Med 1995;333:853-61. doi: 10.1056/NEJM199.509.283331307
23. 23. Stamets K, Taylor DS, Kunselman A, Demers LM, Pelkman CL, Legro RS. A randomized trial of the effects of two typesof short – term hypocaloric diets on weight loss in women with polycystic ovary syndrome. Fertility and Sterility 2004; 81: 630-37. doi:10.1016/j.fertnstert.2003.08.023
24. 24. Douchi T, Ijuin H, Nakamura S, Oki T, Yamamoto S, Nagata Y. Body fat distrubution in women with polycystic ovary syndrome. Obstet Gynecol 1995;86:516-19. doi:10.1016/ S0029-7844(95)80008-5
25. 25. Lefebvre P, Bringer J, Renard E, Boulet F, Clouet S, Jaffiol C. Influences of weight, body fat patterning and nutrition on the manegment of PCOS. Hum Reprod 1997;12:72-81. doi:10.1093/humrep/12.suppl_1.72
26. 26. Kirchengast S, Huber J. Body composition characteristics and body fat distribution in lean women with polycystic ovary syndrome. Hum Reprod 2001;16:1255-60. doi:10.1016/j. fertnstert.2003.08.018
27. 27. Good C, Tulchinsky M, Mauger D, Demers LM, Legro RS. Bone mineral density and body composition in lean women with polycystic ovary syndrome. Fertil Steril 1999;72:21-5. doi:10.1016/S0015-0282(99)00203-4
28. 28. Lord J, Thomas R, Fox B, Acharya U, Wilkin T. The central issue? Visceral fat mass is a good marker of insulin resistance and metabolic disturbance in women with polycystic ovary syndrome. BJOG 2006;113:1203-9. doi:10.1111/j.1471- 0528.2006.00973.x
29. 29. Yücel A, Noyan V, Sagsoz N. The association of serum androgens and insulin resistance with fat distrubution in polycystic ovary syndrome. Eur J Obstet Gynecol Reprod Biol 2006.1;126:81-6. doi:10.1016/j.ejogrb.2005.11.012
30. 30. Clark JT, Kalra PS, Crowley WR. Neuropeptide Y and human pancreatic polypeptide stimulate feeding behavior in rats. Endocrinology 1984; 115: 427-29. doi:10.1210/endo- 115-1-427
31. 31. Arora S, Anubhuti. Role of neuropeptides in appetite regulation and obesity-a review. Neuropeptides 2006; 40: 375-401. doi:10.1016/j.npep.2006.07.001
32. 32. Mircea CN, Lujan ME, Pierson RA. Metabolic fuel and clinical implications for female production. J Obstet Gynaecol Can 2007; 29:887-902. doi: 10.1016/S1701- 2163(16)32661-5.
33. 33. Zarjevski N, Cusin I, Vettor R, Rohner F, Jeanrenaud B. Chronic intracerebroventricular neuropeptide Y administration to normal rats mimics hormonal and metabolic changes of obesity. Endocrinology 1993;133:1753-8. doi:10.1210/endo.133.4.8404618
34. 34. Zarjevski N, Cusin I, Vettor R, Rohner-Jeanrenaud F, Jeanrenaud B. Intracerebroventricular administration of neuropeptide Y to normal rats has divergent effects on glucose utilization by adipose tissue and skeletal muscle. Diabetes 1994;43:764-9. doi:10.1007/s001250051
35. 35. Bennet WM, Wang ZL, Jong P, et al. Presence of neuropeptide Y and its messenger ribonucleic acid in human islets: evidence for a possible paracrine role. J Clin Endocrinol Metab 1996;81:2117-20. doi:10.1210/jcem.81.6.8964837
36. 36. Baranowska B, Radzikowska M, Wasilewska-Dziubinska E, Kaplinski A, Roguski K, Plonowski A. Neuropeptide Y, leptin, galanin and insulin in women with polycystic ovary syndrome. Gynecol Endocrinol 1999;13:344-51. doi:10.3109/095.135.99909167578
37. 37. Gunes M, Bukan N. Examination of angiopoietin-like protein 4, neuropeptide Y, omentin-1 levels of obese and non-obese patients with polycystic ovary syndrome. Gynecol Endocrinol 2015;31:903-6. doi: 10.3109/09513590.2015.1068285.
38. 38. Orbetzova MM, Koleva DI, Mitkov MD, et al. Adipocytokines, neuropeptide Y and insulin resistance in over-weight women with gynoid and android of adipose tissue distribution. Folia Medica 2012:54:22-9. doi:10.2478/v10153.011.0093-7
39. 39. Hatch R, Rosenfield RL, Kim MH, Tredway D. Hirsutism: implications, etiology, and management. Am J Obstet Gynecol 1981;140:815-30. doi: 10.1016/0002-9378(81)90746-8
40. 40. Gennarelli G, Holte J, Stridsberg M, Niklasson F, Berne C, Backstrom T. The counter regulatory response to hypoglycaemia in women with the polycystic ovary syndrome. Clin Endocrinol (Oxf) 1997;46:167-74. doi:10.1046/j.1365- 2265.1997.107.0915.x