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    Comparison of asprosin immunoreactivity in endometrial hyperplasia and grade-1 endometrial adenocarcinoma: A retrospective case-control study
    (Galenos Publ House, 2025) Senocak, Ahmet; Yavuzkir, Seyda; Atilgan, Remzi; Yurt, Nurdan; Balta, Hilal; Kuloglu, Tuncay; Cim, Bunyamin
    Objective: It has been demonstrated that asprosin, a glucogenic adipokine released by white adipose tissue, contributes to the pathophysiology of cancer and disorders associated with it. The aim of this study was to compare the immunoreactivity of asprosin in grade I endometrial adenocarcinoma and in endometrial hyperplasia (EH) with and without atypia. Materials and Methods: A total of 80 cases previously diagnosed with grade 1 endometrial adenocarcinoma and EH with and without atypia, and for which paraffin blocks were obtained, were included in the study. The resulting paraffin blocks were sectioned again and immunostained for asprosin. A total of 80 cases were divided into 4 groups according to their histopathological diagnoses. Group (G) 1 (n=20): proliferative endometrium, G2 (n=20): EH without atypia, G3 (n=20): EH with atypia, G4 (n=20): Grade 1 endometrial adenocarcinoma. Endometrial samples from 80 patients were sectioned, and asprosin immunoreactivity was evaluated by immunohistochemical staining under a light microscope. Results: In comparison to the proliferative endometrium group, the grade I endometrial adenocarcinoma group had considerably increased asprosin immunoreactivity. However, between the proliferative endometrium group and the groups with endometrial hyperplasia, without atypia, and endometrial hyperplasia, with atypia, there was no significant difference in asprosin immunoreactivity. Conclusion: While asprosin immunoreactivity scores are higher in grade I endometrial adenocarcinomas, they are similar to those of the proliferative endometrium in cases of EH with and without atypia, suggesting that energy metabolism contributes to the development of cancer arising from endometrial hyperplasia. Asprosin immunoreactivity can be studied as a marker to predict the progression of EH to cancer.
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    Effects of irisin and exercise on adropin and betatrophin in a new metabolic syndrome model
    (Taylor & Francis Ltd, 2024) Aydin, Suna; Kilinc, Faruk; Ugur, Kader; Aydin, Mustafa Ata; Yalcin, Mehmet Hanifi; Kuloglu, Tuncay; Aydin, Suleyman
    Metabolic syndrome (MetS) is a prevalent public health problem. Uric acid (UA) is increased by MetS. We investigated whether administration of UA and 10% fructose (F) would accelerate MetS formation and we also determined the effects of irisin and exercise. We used seven groups of rats. Group 1 (control); group 2 (sham); group 3 (10% F); group 4 (1% UA); group 5 (2% UA); group 6 (10% F + 1% UA); and Group 7, (10% F + 2% UA). After induction of MetS (groups 3 -7), Group 3 was divided into three subgroups: 3A, no further treatment; 3B, irisin treatment; 3C, irisin treatment + exercise. Group 4, 1% UA, which was divided into three subgroups: 4A, no further treatment; 4B, irisin treatment; 4C, Irisin treatment + exercise. Group 5, 2% UA, which was divided into three subgroups: 5A, no further treatment; 5B, irisin treatment; 5C, irisin treatment + exercise. Group 6, 10% F + 1% UA, which was divided into three subgroups: 6A, no further treatment; 6B, irisin treatment; 6C, irisin treatment + exercise. Group 7, 10% F + 2% UA, which was divided into three subgroups: 7A, no further treatment; 7B, irisin treatment; 7C, irisin treatment + exercise., Irisin was administered 10 ng/kg irisin intraperitoneally on Monday, Wednesday, Friday, Sunday each week for 1 month. The exercise animals (in addition to irisin treatment) also were run on a treadmill for 45 min on Monday, Wednesday, Friday, Sunday each week for 1 month. The rats were sacrificed and samples of liver, heart, kidney, pancreas, skeletal muscles and blood were obtained. The amounts of adropin (ADR) and betatrophin in the tissue supernatant and blood were measured using an ELISA method. Immunohistochemistry was used to detect ADR and betatrophin expression in situ in tissue samples. The duration of these experiments varied from 3 and 10 weeks. The order of development of MetS was: group 7, 3 weeks; group 6, 4 weeks; group 5, 6 weeks; group 4, 7 weeks; group 3, 10 weeks. Kidney, liver, heart, pancreas and skeletal muscle tissues are sources of adropin and betatrophin. In these tissues and in the circulation, adropin was decreased significantly, while betatrophin was increased significantly due to MetS; irisin + exercise reversed this situation. We found that the best method for creating a MetS model was F + UA2 supplementation. Our method is rapid and simple. Irisin + exercise was best for preventing MetS.