Objective: The pathogenesis of endometriosis has not been clearly explained. Inflammatory factors of ectopic implantation and the growth of ectopic endometrial cells have been subjects of major interest. The number of studies evaluating salusin-α and nesfatin-1 markers in patients with endometriosis is limited. No studies have evaluated the levels of anti-inflammatory markers for adropin and netrin-1 in patients with endometriosis. This study investigates how some important inflammatory regulatory markers in the inflammatory process affect the pathogenesis of endometriosis and determines whether any relationship exists between serum levels of these parameters and endometriosis and insulin resistance.
Materials And Methods: This prospective study included 73 patients with endometriosis diagnosed histopathologically after laparoscopic surgery and 75 healthy controls. Serum adropin, salusin-α, netrin-1, and nesfatin-1 levels and homeostatic model assessment of insulin resistance (HOMA-IR) values of the participants were measured.
Results: The endometriosis group had significantly lower nesfatin-1 levels than the control group (3.0±0.53 vs 9.5±0.94, p=0.005). Between the patient and control groups, there was no difference regarding serum adropin, salusin-α, and netrin-1 levels (p=0.36, p=0.34, p=0.75, respectively). Nesfatin-1 had a significant positive correlation with adropin, salusin-α, and netrin-1 (r=0.563, p<0.01; r=0.738, p<0.01; r=0.700, p<0.01, respectively), but had a negative correlation with fasting blood glucose (r=-0.343, p<0.05). HOMA-IR values were comparable between both groups.
Conclusion: The lower nesfatin-1 levels leading to increased inflammatory pathway activity in patients with endometriosis might play a role in endometriosis pathogenesis. Without causing systemic insulin resistance, decreased nesfatin-1 might contribute to endometriosis pathogenesis locally by leading to the reduced insulin susceptibility of endometriosis cells.
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| http://dx.doi.org/10.4274/tjod.galenos.2021.12080 | DOI Listing |
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