Polikistik Over Sendromunun Patogenezinde Progranulin ve Tnf-Alfa Nın Rolü
Uzdoğan, Esma Andaç
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Polycystic ovary syndrome (PCOS) is chacterized by menstrual irregularities, hirsutism, acne and obesity. Chronic and subclinic inflammation, insulin resistance are the basic pathological mechanisms of PCOS. Tumor necrosis factor-alpha (TNF-alpha) released from inflammatory cells and adipose tissue is known to play a role in the pathogenesis of inflammatory disease, insulin resistance and PCOS. According to the recent publications, progranulin (PGRN), which is released from adipose tissue, is suggested to use TNF-alpha receptors and has anti-inflammatory effects. PGRN is a 68-88 kDa glycoprotein and a member of the groups of autocrine growth factors. In this study, we aimed to investigate the role of PGRN and TNF-alpha in the pathogenesis of PCOS and the interaction of the molecules with each other. Additionally, we planned to measure total oxidant status (TOS), total anti-oxidant status (TAOS), dehydroepiandrosterone sulphate (DHEAS) and paraoxonase 1 (PON1) enzyme activities in PCOS patients and compare to the control group. For this purpose, PGRN and TNF-alpha serum levels were measured in 40 PCOS patient and 40 healthy control group. Serum PGRN and TNF-alpha were significiantly higher in patients with PCOS compared with the control group (p=0.037, p=0.041). In addition, both groups were shown to correlate with increases in PGRN and TNF-alpha. TOS level was higher in control group, TAOS level was higher in the PCOS patient group and DHEAS level increased with TAOS level in a paralel manner. PON1 activity, found on the high density lipoprotein (HDL), was higher in PCOS patients than the control group and the difference was statistically significiant (0.009). The parallel increase of PGRN and TNF-alpha serum levels in the PCOS patients and the fact that they are using the same receptor suggest that there is a competition between PGRN and TNF-alpha at the receptor level. The increase in PGRN may have a protective effect against TNF-alpha at the molecular level in the pathogenesis of PCOS.