OBESITY IN PATIENTS WITH POLYCYSTIC OVARY SYNDROME. PATHOGENETIC ASPECTS AND PERSPECTIVE DIRECTIONS OF THERAPY

Authors

  • Goncharova O. A. Kharkiv National Medical Univercity, Kharkiv, Ukraine; SI «Danilevsky Institute for Endocrine Pathology Problems of the National Academy of Medical Sciences of Ukraine», Kharkiv, Ukraine https://orcid.org/0000-0001-5864-5686
  • Arkhypkina T. L. SI «Danilevsky Institute for Endocrine Pathology Problems of the National Academy of Medical Sciences of Ukraine», Kharkiv, Ukraine https://orcid.org/0000-0001-5529-7583
  • Liubymova L. P. SI «Danilevsky Institute for Endocrine Pathology Problems of the National Academy of Medical Sciences of Ukraine», Kharkiv, Ukraine https://orcid.org/0000-0003-2984-6969

DOI:

https://doi.org/10.21856/j-PEP.2022.2.15

Keywords:

obesity, polycystic ovary syndrome, metformin, liraglutide

Abstract

Polycystic ovary syndrome (PCOS) is a common endocrine disorder with a complex multifactorial pathogenesis, largely associated with android-type obesity (Ob). Ob and overweight, which occurs in 50-80 % of PCOS patients, not only affects overall health but also impairs reproductive function, steroid metabolism with increased levels of free androgens, and due to peripheral androgen conversion - and an increase in estrogen levels. Androgens increase lipolysis with the accumulation of additional free fatty acids and the development of atherogenic dyslipidemia. Almost 90-100% of patients with Ob have insulin resistance (IR), against which develops compensatory hyperinsulinemia (GI). In general, Ob, IR, and secondary GI affect the full range of disorders associated with PCOS. Therefore, an important step in the treatment of PCOS is to reduce the total mass of adipose tissue, and in this, in addition to lifestyle modifications, the leading role is played by drug therapy. Today, the most common used drug in the treatment of reproductive pathology in women with PCOS and Ob in the presence of IR is metformin. Literature data and practical experience conducted at the clinic of IPEP with a survey of 128 women with the classical phenotype of PCOS and Ob by android type, GI and IR indicate that metformin therapy leads to lower serum glucose, increased sensitivity of peripheral tissues to insulin improving the lipid spectrum of the blood, lowering triglycerides, increasing the globulin that binds sex hormones, reducing hyperandrogenemia. At the same time, there was just a tendency to reduce the body mass index, waist-to-hip ratio and the specific gravity of fat. That is, the effect of metformin on weight loss and adipose tissue distribution was insufficient. For today, it is considered appropriate to use glucagon-like peptide 1 (GLP-1) agonists in patients with PCOS with Ob and IR, which lead to a more significant decrease in body mass index and waist circumference compared to metformin. There are data on a significant improvement in metabolic and hormonal parameters, as well as the restoration of menstrual cycles after the use of combination therapy with GLP-1 agonist and metformin. This combination also makes it possible to use lower doses of both drugs, which is not accompanied by a significant difference in the frequency and severity of possible side effects compared with monotherapy with GLP-1 agonist or metformin.

References

Conway G, Dewailly D, Diamanti-Kandarakis E, et al. Reprod Endocrinol 2015;25: 32-52. http://doi.org/10.18370/2309-4117.2015.25.32-52.

Bizoń A, Franik G, Niepsuj J, et al. Clin Med 2021;10(17): 3941. http://doi.org/10.3390/jcm10173941.

Ma Ruilin, Ding Xuesong, Wang Yanfang, et al. Medicine 2021;100(23): e26295. http://doi.org/10.1097/MD.0000000000026295.

Lim SS, Davies MJ, Norman RJ, Moran LJ. Hum Reprod Update 2012;18(6): 618-637. http://doi.org/10.1093/humupd/dms030.

Yildiz BO. Women’s Health 2013;9: 505-507. http://doi.org/10.2217/WHE.13.53.

Shishehgar F, Tehrani FR, Mirmira P, et al. PLoS One 2016;11(10): 1-11. http://doi.org/10.1371/journal.pone.0162911.

Cena H, Chiovato L, Nappi RE. J Clin Endocrinol Metab 2020;105(8): e2695-e2709. http://doi.org/10.1210/clinem/dgaa285.

Chen J, Shen S, Tan Y, et al. J Ovarian Res 2015;8: 11. http://doi.org/10.1186/s13048-015-0139-1.

Reinehr T, Kulle A, Rothermel J, et al. Endocr Connect 2017;6(4): 213-224. http://doi.org/10.1530/EC-17-0051.

Pasquali R, Gambineri A, Pagotto U. BJOG 2006;113(10): 1148-1159. http://doi.org/10.1111/j.1471-0528.2006.00990.x.

Xu XF, De Pergola G, Bjorntorp P. Endocrinology 1991;128(1): 379-382. http://doi.org/10.1210/endo-128-1-379.

Dumesic DA, Akopians AL, Madrigal VK, et al. J Clin Endocrinol Metab 2016;101(11): 4178-418. http://doi.org/10.1210/jc.2016-2586.

Sıklar Z, Berberoğlu M, Camtosun EKocaay P. J Pediatr Adolesc Gynecol 2015;28(2): 78-83. http://doi.org/10.1016/j.jpag.2014.05.006.

Legro RS, Castracane VD, Kauffman RP. Obstet Gynecol Surv 2004;59(2): 141-154. http://doi.org/10.1097/01.OGX.0000109523.25076.E2

Diamanti-Kandarakis E, Xyrafis X, Boutzios G. Panminerva Med 2008;50(4): 315-325.

Sozen I, Arici A. Obstet Gynecol Surv 2000;55(5): 321-328. http://doi.org/10.1097/00006254-200005000-00026.

Scott EE, Wolf CR, Otyepka M, et al. Drug Metab Dispos 2016;44(4): 576-590.http://doi.org/10.1124/dmd.115.068569.

Rosenfield RL, Ehrmann DA. Endocrin Rev 2016;37(5): 467-520. https://doi.org/10.1210/er.2015-1104.

Jeanes YM, Reeves S. Nutr Res Rev 2017;30(1): 97-105. http://doi.org/10.1017/S0954422416000287.

Moran LJ, Hutchison SK, Norman RJ, Teede HJ. Cochrane Database Systematic Rev 2011;16(2). http://doi.org/10.1002/14651858.

Matsuzaki T, Tungalagsuvd A, Iwasa T, et al. Reprod Med Biol 2017;16(2): 179-187. http://doi.org/10.1002/rmb2.12026.

Livadas S, Anagnostis P, Bosdou JK, et al. World J Diabetes 2022; 13(1): 5-26. http://doi.org/10.4239/wjd.v13.i1.5.

Bredella MA, McManus S, Misra M. Clin Endocrinol (Oxf) 2013;79: 199-203. http://doi.org/10.1111/cen.12028

Palomba S, Falbo A, Russo T, et al. Hum Reprod 2010;25(4): 1005-1013. http://doi.org/10.1093/humrep/dep466.

Arkhypkina TL. J Clin Experim Med Res 2013;4(7): 445-451.

Lyseng-Williamson KA. Clin Drug Invest 2019;39(8): 805-819. http://doi.org/10.1007/s40261-019-00826-0.

Kushnarova NM, Zinych OV, Korpavchev VV. Mìžnar Endokrinol Žurn 2021;17(8): 637-645.http://doi.org/10.22141/2224-0721.17.8.2021.246799.

Sever MJ, Kocjan T, Pfeifer M, et al. Eur J Endocrinol 2014;170(3): 451-459. http://doi.org/10.1530/EJE-13-0797.

Vilsbøll T, Christensen M, Anders E, et al. BMJ 2012;344. http://doi.org/10.1136/bmj.d7771.

Jensterle M, Kocjan T, Kravos NA, et al. Endocr Res 2015;40(3): 133-138. http://doi.org/10.3109/07435800.2014.966385.

Frøssing S, Nylander M, Chabanova E, et al. Diabetes Obes Metab 2018;20(1): 215-218. http://doi.org/10.1111/dom.13053.

Papaetis GS, Filippou PK, Constantinidou KG, Stylianou CS. Clin Drug Investig 2020;40(8): 695-713. http://doi.org/10.1007/s40261-020-00942-2.

Nylander M, Frøssing S, Clausen HV, et al. Reprod Biomed Onlin 2017;35(1): 121-127. http://doi.org/10.1016/j.rbmo.2017.03.023.

Jensterle M, Goricar K, Janez A. Exp Ther Med 2016;11(4): 1194-1200. http://doi.org/10.3892/etm.2016.3081.

Ge JJ, Wang DJ, Song W. J Endocrinol Invest 2022;45(2): 261-273. http://doi.org/10.1007/s40618-021-01666-6.

Maida A, Lamont BJ, Cao X, Drucker DJ. Diabetologia 2011;54(2): 339-349. http://doi.org/10.1007/s00125-010-1937-z.

Ruilin M, Xuesong D, Yanfang W, et al. Medicine 2021;100(23): e26295. http://doi.org/10.1097/MD.0000000000026295.

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Published

2022-06-09

How to Cite

Гончарова, О., Архипкіна, Т., & Любимова, Л. (2022). OBESITY IN PATIENTS WITH POLYCYSTIC OVARY SYNDROME. PATHOGENETIC ASPECTS AND PERSPECTIVE DIRECTIONS OF THERAPY . Problems of Endocrine Pathology, 79(2), 105-111. https://doi.org/10.21856/j-PEP.2022.2.15

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