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Öğe Adropin: a key component and potential gatekeeper of metabolic disturbances in policystic ovarian syndrome(7847050 Canada Inc, 2014) Yildirim, B.; Celik, O.; Aydin, S.Purpose: The aim of the current study was to evaluate potential relationships between serum adropin levels and metabolic parameters in polycystic ovary syndrome (PCOS). Materials and Methods: Twenty women with PCOS and 20 healthy, age and body mass index (BMI) matched controls were included in the study. All subjects underwent venous blood drawing on the early follicular phase after an overnight fasting. Serum adropin levels were measured with enzyme immunosorbent assay (ETA). The relationships between serum adropin levels and metabolic parameters were also assessed. Results: Serum adropin levels were found to be significantly lower in women with PCOS when compared to control group (p < 0.001). Serum adropin level was correlated negatively with fasting serum insulin levels, homeostasis model of assessment - insulin resistance (HOMA-IR) and serum lipid markers including cholesterol, very low-density lipoprotein, and triglycerides (TG) in PCOS patients (p < 0.05). Conclusion: The findings of current study suggest that women with PCOS have low serum adropin levels that may contribute to the underlying pathogenesis of metabolic disturbances in PCOS.Öğe An appraisal on serum preptin levels in polycystic ovary syndrome(Oxford Univ Press, 2010) Celik, O.; Hascalik, S.; Celik, N.; Sahin, I.; Aydin, S.[Abstract Not Available]Öğe Bacterial Translocation in Experimental Acute Necrotizing Pancreatitis: Effects of Infliximab(Lippincott Williams & Wilkins, 2010) Aydin, S.; Isik, A. T.; Unal, B.; Comert, B.; Ozyurt, M.; Deveci, S.; Erdem, G.[Abstract Not Available]Öğe Does hepcidin play a role in the pathogenesis of aphthae in Behcet's disease and recurrent aphthous stomatitis?(Wiley, 2014) Cicek, D.; Dagli, A. F.; Aydin, S.; Dogan, F. Baskaya; Dertlioglu, S. B.; Ucak, H.; Demir, B.BackgroundAphthae constitute one of the major signs in Behcet's disease (BD) and recurrent aphthous stomatitis (RAS). No scientific study has yet explored the relationship of hepcidins, which have antimicrobial effects, with RAS and BD. ObjectivesIn this study, we aimed to evaluate by immunohistochemistry whether hepcidin is synthesized by the salivary glands and to measure levels of prohepcidin and hepcidin (an antibacterial peptide) in the serum and saliva of patients with BD and RAS. MethodsThe study included 25 BD patients and 30 RAS patients, as well as a control group comprising 25 healthy individuals. Serum and saliva samples were collected at the same time from all subjects. Levels of prohepcidin and hepcidin were measured by ELISA. The presence of hepcidin in salivary glands was assessed by immunohistochemistry. ResultsHepcidin was localized in the striated ducts of the sublingual and parotid glands. Saliva prohepcidin and hepcidin levels were correlated with blood levels. Saliva prohepcidin levels were found to be lower in RAS patients than in BD patients and healthy controls (P<0.001 and P=0.007 respectively). In addition, RAS patients had lower saliva hepcidin levels than did the control group (P=0.03). ConclusionsThe lower serum and saliva prohepcidin and hepcidin concentrations found in RAS and BD patients indicate that hepcidin may be involved in the aetiopathogenesis of these diseases. Because it can be obtained non-invasively and easily, saliva may provide a useful alternative to serum in quantifying prohepcidin and hepcidin concentrations.Öğe Molecular communication between Apelin-13 Apelin-36, Elabela, and nitric oxide in gestational diabetes mellitus(Verduci Publisher, 2022) Karagoz, Z. K.; Aydin, S.; Ugur, K.; Tigli, A.; Deniz, R.; Baykus, Y.; Sahin, IOBJECTIVE: Gestational diabetes mellitus (GDM) is a type of diabetes that affects from 3.8% to 6.9% of pregnancies worldwide, causing significant mortality and unfavorable obstetric outcomes. such as delivery trauma and macrosomia risk. The fundamental processes of this metabolic disorder that first appeared during pregnancy are still unknown. Tissue hormones, particularly adipokines. have aided in understanding the pathophysiology of numerous disorders in recent years. This study aims to determine if Apelin-13 (APLN-13), Apelin-36 (APLN-36). Elabela (ELA), and nitric oxide (NO) molecules have all a part in the pathophysiology of GDM. PATIENTS AND METHODS: The study included 30 pregnant control women and 30 pregnant women who had been diagnosed with GDM in the second trimester and whose body mass index and age were compatible with each other. Blood samples were collected from 60 participants during the second trimester (30 control pregnant women and 30 GDM pregnant women) and postpartum (17 controls vs. 14 GDM). In these blood samples, the amounts of APLN-13, APLN-36, ELA, and NO were studied using the ELISA method. In addition, the participants' glucose, lipid profiles, and other parameters were obtained from the hospital record files. At postpartum, 29 pregnant women (13 control and 16 pregnant women with GDM) dropped out of the study without explanation. RESULTS: In the second trimester and postpartum plasma of mothers with GDM. APLN-13, APLN-36. NO. and ELA molecules were found to be significantly higher (< 0.05). compared to those of the control mothers. while APLN-13, APLN-36. NO values were significantly lower (0.05). While APLN-13. APLN-36, NO amounts in mothers with GDM were positively correlated with glucose amounts. they were negatively correlated with ELA amounts. Similarly, the triglyceride amounts in mothers with GDM were positively correlated with APLN-13, APLN-36 and NO, while they were negatively correlated with the ELA amounts. Due to gestational diabetes, APLN-13, APLN-36, NO. glucose. and triglyceride increased. and ELA decreased. CONCLUSIONS: It is predicted that the glucose increase in GDM is because Apelins reduce glucose transport to erythrocytes by inhibiting the sodium-dependent glucose transporter (SGLT) and that the increase in triglyceride and NO may be associated with high glucose levels in GDM. As a result, we believe that the above-mentioned chemicals may cause GDM Pathology by triggering one another.
