RESUMO
OBJECTIVE: 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.
Assuntos
Diabetes Gestacional , Peptídeos e Proteínas de Sinalização Intercelular , Hormônios Peptídicos , Apelina/metabolismo , Glicemia/metabolismo , Comunicação , Diabetes Gestacional/metabolismo , Feminino , Glucose/metabolismo , Humanos , Peptídeos e Proteínas de Sinalização Intercelular/metabolismo , Óxido Nítrico , Hormônios Peptídicos/metabolismo , Gravidez , Triglicerídeos/metabolismoRESUMO
PURPOSE: Central serous chorioretinopathy (CSCR) is an eye disease of unknown etiology that presents with reduced visual acuity, choroidal thickening (distance between Bruch's membrane and the chorioscleral border), and subretinal fluid leakage. In the present study, the goal was to investigate the role of the interrelated tenascin C, metalloprotein-1, BAX, BCL2, subfatin and asprosin molecules in the pathogenesis of CSCR. METHOD: Thirty CSCR patients and 30 controls were included. CSCR was diagnosed by optical coherence tomography imaging. A 5mL blood sample was collected from all participants after overnight fasting. Compounds in the blood samples were studied with the Enzyme-Linked Immunosorbent Assay (ELISA) method. RESULTS: Patients with CSCR were found to have macular thickening (P: 0.08) and statistically significantly reduced visual acuity (P: 0.034) compared to controls. With regard to serum parameters, there were statistically significant increases in tenascin C, metalloprotein-1, BAX, BCL2, subfatin and asprosin levels compared to controls. We found a positive correlation between macular thickness and tenascin C (r+0.670, P<0.001), metaloprotein-1 (r+0.714, P<0.001), BAX, BCL2 (r+0.771, P<0.001), subfatin and asprosin levels and a negative correlation between visual acuity and tenascin C (r+0.605 P<0.001), metaloprotein-1 (r+0.704, P<0.001), BAX, BCL2 (r+0.738, P<0.001), subfatin and asprosin levels. CONCLUSION: The molecules studied herein were negatively correlated with visual acuity and positively correlated with macular thickness, suggesting that these molecules might have a role in the pathogenesis of CSCR. Thus, we predict that these molecules could be new candidates for the diagnosis and follow-up of CSCR in the future.
Assuntos
Coriorretinopatia Serosa Central , Metaloproteínas , Coriorretinopatia Serosa Central/diagnóstico , Coriorretinopatia Serosa Central/patologia , Angiofluoresceinografia/métodos , Humanos , Laboratórios , Proteínas Proto-Oncogênicas c-bcl-2 , Estudos Retrospectivos , Tenascina , Tomografia de Coerência Óptica/métodos , Proteína X Associada a bcl-2RESUMO
We investigated the expression of irisin in renal cancers using immunocytochemistry. Irisin has been reported to exhibit anticancer properties. The study groups consisted of 22 cases each of control renal tissue, oncocytoma, chromophobe renal cell carcinoma (RCC), clear cell RCC (Fuhrman nuclear grades 1, 2, 3 and 4) and papillary RCC. We evaluated 10 slides for each of 176 cases. Slides were immunostained for irisin and histoscores were calculated for the prevalence and strength of immunostaining. Fuhrman nuclear grade 1, 2, 3 clear cell RCC and papillary RCC exhibited no irisin immunoreactivity. Irisin immunoreactivity was observed in some Fuhrman nuclear grade 4 RCCs. We found a significant decrease in irisin staining in chromophobe RCC compared to the control. Immunoreactivity in the oncocytoma tissue was comparable to the control group. Irisin immunoreactivity in chromophobe RCC decreased and no immunoreactivity was observed in Fuhrman nuclear grade 1, 2, 3 clear cell RCC and papillary RCC. Immunistochemical screening of irisin in renal oncocytomas and renal cancers may be useful for differential diagnosis.