Polycystic ovary syndrome is known to be the most common hormonal disorder in women of reproductive age. Current evidence shows that regulatory proteins secreted from the adipose tissue called adipokines may have a role in polycystic ovary syndrome. We planned to investigate the role of endotrophin that has never been researched in polycystic ovary syndrome before and its correlation with other metabolic parameters and adipokines such as adiponectin and ghrelin in patients with polycystic ovary syndrome. Forty-three women (n: 43) with polycystic ovary syndrome and 43 (n: 43) women as a control group were enrolled in this cross-sectional study. Serum levels of endotrophin, adiponectin, and ghrelin levels were measured with the enzyme-linked immunosorbent assay method. High-density lipoprotein cholesterol, low-density lipoprotein cholesterol, total cholesterol levels, luteinizing hormone/follicle-stimulating hormone ratio, total testosterone, and triglyceride levels were measured. Homeostasis model assessment for insulin resistance index, body mass index, Ferriman Gallwey Score, and waist-to-hip ratio were also evaluated. Total testosterone, homeostasis model assessment for insulin resistance, C-reactive protein, luteinizing hormone/follicle-stimulating hormone ratio, and triglyceride levels were higher in patients with polycystic ovary syndrome (p < 0.01). No difference was detected between the groups in terms of body mass index, Ferriman Gallwey Score, waist-to-hip ratio, total cholesterol, low-density lipoprotein, and high-density lipoprotein levels (p > 0.05). We did not observe any significant difference in adiponectin and ghrelin levels between the groups (p > 0.05). Patients with polycystic ovary syndrome had significantly higher endotrophin levels (p < 0.01). According to our regression analyses [area under the curve: 0.973 (0.935–1.000), 95% confidence interval, 95.2% sensitivity, and 100% specificity], it was shown that endotrophin greater than 92 ng/ml and homeostasis model assessment for insulin resistance greater than 2.5 might be good predictors for polycystic ovary syndrome diagnosis. We demonstrated that endotrophin level is higher in patients with polycystic ovary syndrome and may have predicted polycystic ovary syndrome with increased homeostasis model assessment for insulin resistance index. There was no significant difference in adiponectin and ghrelin levels in the polycystic ovary syndrome group. Endotrophin may have a role in polycystic ovary syndrome etiology rather than other adipokines.

Background: Ovulation is regulated by extracellular signal-regulated kinase-1 (ERK-1) and ERK-2 signaling mechanisms, and ERK-1/2 kinases modulates the function of most of the LH-regulated genes. Defective ERK kinase signaling that is secondary to a genetic problem contributes to both ovulatory dysfunction and metabolic problems in polycystic ovary syndrome (PCOS). We planned to investigate ERK-1 and ERK-2 gene polymorphisms in PCOS for the first time in the Turkish population. Methods: One hundred two PCOS patients and 102 healthy controls were recruited for this patient control study. HOMA-IR, Ferriman-Gallwey score (FGS), waist-to-hip ratio (WHR), and body mass index (BMI) were assessed. Lipid profile levels, CRP, and total testosterone were determined. ERK-2 rs2276008 (G > C) and ERK-1 rs11865228 (G > A) SNPs were analyzed with a real-time PCR system. Results: ERK-1 and ERK-2 genotypes were found to differ between the PCOS and control groups. In patients with PCOS, ERK-1 GA and ERK-2 GC genotypes were different in terms of BMI, FGS, HOMA-IR, CRP, total testosterone, and total cholesterol levels. Conclusions: ERK-1 and ERK-2 genes are involved in PCOS pathogenesis. BMI, FGS, HOMA-IR, and CRP levels are related to the heterozygote polymorphic types of ERK-1 and ERK-2 genes.

Background: Oncostatin M, a novel adipokine, plays a role in oogenesis, lipogenesis, and inflammation and may contribute to polycystic ovary syndrome pathogenesis and related metabolic problems. Adipokines are believed to contribute to developing polycystic ovary syndrome and its accompanying metabolic parameters, such as dyslipidemia, insulin resistance, and cardiovascular diseases. Methods: In this case–control study, the patients were grouped in a 1:1 ratio into either the polycystic ovary syndrome (n = 32) or the control group (n = 32). Serum levels of fasting glucose, insulin, C-reactive protein, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglyceride, white blood cell count, thyroid-stimulating hormone, luteinizing hormone, follicle-stimulating hormone, total testosterone, prolactin, estradiol, homeostasis model assessment of insulin resistance, and oncostatin M were analyzed. Results: Oncostatin M levels were significantly lower, but C-reactive protein levels were substantially higher in the polycystic ovary syndrome group than in the control group (p = 0.002, p = 0.001, respectively). Oncostatin M was inversely correlated with total cholesterol, non-high-density lipoprotein cholesterol, fasting glucose, and the luteinizing hormone/follicle-stimulating hormone ratio (ρ = −0.329, p =0.017; ρ = −0.386, p = 0.005; ρ = −0.440, p = 0.001; ρ = −0.316, p = 0.023, respectively). Conversely, there was no correlation between oncostatin M and total testosterone level (ρ = 0.220; p = 0.118). In the context of inflammation and metabolic parameters, oncostatin M was inversely correlated with C-reactive protein, homeostatic model assessment for insulin resistance score, and low-density lipoprotein cholesterol (ρ = −0.353, p = 0.019; ρ = −0.275, p = 0.048; ρ = −0.470, p < 0.001, respectively). Conclusions: Plasma oncostatin M levels were considerably lower in patients with polycystic ovary syndrome than in the control group, and this was inversely correlated with the hormonal and metabolic parameters of polycystic ovary syndrome. Thus, oncostatin M may be a novel therapeutic target for polycystic ovary syndrome and its metabolic parameters.

Neutrophil gelatinase-associated lipocalin (NGAL, also known as lipocalin-2) is an acute-phase protein expressed in many tissues and plays a role in cell proliferation, regulation, and epithelial-mesenchymal transformation. Therefore, this study aimed to investigate serum NGAL levels and endometrioma tissue expression in women with endometriosis. This cross-sectional study was conducted at a university hospital. The endometrioma group included 36 women who underwent ovarian cystectomy for endometrioma, which was compared with a control group (n = 36) of women who underwent ovarian cystectomy due to benign persistent cysts (follicle cyst, theca lutein cyst, and serous cystadenoma). NGAL levels were analyzed using both serum enzyme-linked immunosorbent assay analysis and immunohistochemical tissue staining. Serum C-reactive protein and CA-125 levels were also evaluated. NGAL serum levels were significantly higher in the endometrioma group than in the control group (P < .05). C-reactive protein and CA-125 levels were also significantly higher in the endometrioma group (P < .05) and were correlated with NGAL levels. Immunohistochemical staining for NGAL was also higher in the endometrioma group (P < .001). NGAL may be considered a potential noninvasive biomarker of endometriosis.

Introduction The aim of this study was to compare serum vitamin D and osteocalcin levels in non-osteoporotic postmenopausal women with and without metabolic syndrome and to analyze the relationship between serum vitamin D and osteocalcin levels and the relationships between these two factors and other clinical/biochemical parameters. Material and Method This cross-sectional study was carried out in 191 postmenopausal non-osteoporotic (T-score > − 2.5) women. Patients were divided into two groups according to the presence or absence of metabolic syndrome. Blood samples were obtained and evaluated for 25-hydroxyvitamin D, osteocalcin, insulin resistance (using a homeostatic model assessment of insulin resistance), glycosylated hemoglobin (HbA_1c), calcium, phosphorus, deoxypyridinoline, thyroid-stimulating hormone, lipid profile, fasting insulin, fasting glucose and HbA_1c levels. Demographic and laboratory parameters were recorded for each woman. Results Vitamin D was found to be lower in women with metabolic syndrome compared to controls (16.1 ± 11.2 vs. 20.4 ± 13.1 mg/dL; p = 0.013). Similarly, osteocalcin was found to be significantly lower in the metabolic syndrome group compared to the control group (4.2 ± 2.1 vs. 5.5 ± 3.0; p < 0.001). A significant positive correlation was observed between vitamin D and osteocalcin levels (r = 0.198; p = 0.008). There was an inverse correlation between vitamin D and some of the lipid parameters. However, osteocalcin levels were negatively correlated with C-reactive protein, insulin resistance, and HbA_1c in both groups (p = 0.003, p = 0.001 and p = 0.048, respectively). Conclusion Vitamin D deficiency is common in postmenopausal women, even in women who are non-osteoporotic. Serum levels of vitamin D are significantly decreased in cases with metabolic syndrome. Vitamin D may directly improve serum lipid profiles and may indirectly decrease insulin resistance and subclinical systemic inflammation through the impact on the metabolic functions of osteocalcin. Einleitung Ziel dieser Studie war es, die Vitamin-D- und Osteocalcin-Blutwerte bei Frauen ohne Osteoporose nach der Menopause mit und ohne metabolischem Syndrom zu vergleichen und die Beziehungen zwischen Vitamin D und Osteocalcin sowie zwischen diesen beiden Faktoren und anderen klinischen und biochemischen Parametern zu analysieren. Material und Methode Diese Querschnittsstudie wurde bei 191 Frauen ohne Osteoporose (T-Score > − 2,5) nach der Menopause durchgeführt. Die Patientinnen wurden in 2 Gruppen eingeteilt, je nach Vorhandensein oder Abwesenheit eines metabolischen Syndroms. Allen Frauen wurden Blutproben entnommen und auf 25-Hydroxy-Vitamin D, Osteocalcin, Insulinresistenz (basierend auf ein homöostatisches Modell zur Beurteilung der Insulinresistenz), glykosyliertes Hämoglobin (HbA_1c), Kalzium, Phosphor, Desoxypyridinolin, Thyreotropin, Lipidprofil, Nüchternblutzucker, Nüchternglukosewerte sowie die HbA_1c-Werte untersucht. Die gewonnenen demografischen und Laborwerte wurden für jede der Frauen aufgezeichnet. Ergebnisse Frauen mit einem metabolischen Syndrom wiesen einen niedrigeren Vitamin D-Spiegel auf im Vergleich zur Kontrollgruppe (16,1 ± 11,2 vs. 20,4 ± 13,1 mg/dl; p = 0,013). Auch die Osteocalcin-Werte waren signifikant niedriger in der Gruppe mit metabolischem Syndrom verglichen mit der Kontrollgruppe (4,2 ± 2,1 vs. 5,5 ± 3,0; p < 0,001). Es gab eine signifikante positive Korrelation zwischen Vitamin-D- und Osteocalcin-Werten (r = 0,198; p = 0,008). Vitamin D und einige der Lipidparameter waren invers korreliert. Allerdings gab es eine negative Korrelation in beiden Gruppen zwischen dem Osteocalcin-Spiegel und C-reaktivem Protein, Insulinresistenz und HbA_1c (p = 0,003, p = 0,001 bzw. p = 0,048). Schlussfolgerung Vitamin-D-Mangel kommt häufig vor bei Frauen nach der Menopause, selbst bei Frauen, die keine Osteoporose haben. In Fällen mit metabolischem Syndrom waren die Vitamin-D-Werte im Blut deutlich reduziert. Vitamin D könnte zu einer direkten Verbesserung der Lipidprofilwerte und indirekt zu einem Rückgang der Insulinresistenz und der subklinischen systemischen Entzündung führen, durch dessen Auswirkung auf die metabolische Funktion von Osteocalcin.