The aim of this study was to compare the levels of nesfatin-1 in healthy subjects with those in prediabetic and diabetic patients who have different glucose tolerance levels. Overall, 100 subjects were divided into 5 groups healthy control (C), impaired fasting glycemia (IFG), impaired glucose tolerance (IGT), metabolic syndrome (MS) and type 2 diabetes mellitus, (Type 2 DM). Glycated hemoglobin (HbA1c) assessed the glycemic control. Homeostasis model assessment of insulin resistance (HOMA-IR) was determined using computer analyses. Nesfatin-1 levels were measured using ELISA method. IFG and IGT (prediabetic groups) from MS and Type 2 DM (diabetic groups) differed significantly in HOMA-IR. The nesfatin-1 levels were lower, although not statistically significant, in IFG (0.937±0.03 ng/ml, p=0.07) and IGT (1.039±0.06 ng/ml, p=0.5) groups compared to healthy subjects (1.094±0.07 ng/ml). However, the nesfatin-1 levels were lower in patients with Type 2 DM (0.867±0.02 ng/ml, p=0.007) and MS (0.885±0.01 ng/ml, p=0.01) compared to healthy subjects. Nesfatin-1 levels were significantly lower in diabetic patients compared to healthy subjects. This study supports the role of insulin resistance in decreased nesfatin-1 levels in patients with Type 2 DM and MS.

Objective The goal of this study was to evaluate the importance of nesfatin-1, acylated and des-acylated ghrelin, which are known as energy regulatory hormones, in patients with moderate and severe major depression disorders (MDD). Methods Thirty patients with a moderate degree of MDD and, 30 with a severe degree of MDD were used as participants in this study. Thirty subjects without depression were enrolled as a control group. The Hamilton Depression Rating Scale was used to classify the patients with MDD. Blood samples were taken after overnight fasting. The plasma nesfatin-1, acylated ghrelin and des-acylated ghrelin levels were measured using a commercially available enzyme-linked immunosorbent assay kit. Results The nesfatin-1, the acylated ghrelin and the des-acylated ghrelin levels were found to be significantly higher in severe MDD (3.92±0.4 ng/mL; 88.56±4.1 pg/mL; 962.76±67 pg/mL) as compared to moderate MDD (2.91±0.5 ng/mL; 77.63±4.19 pg/mL; 631.16±35 pg/mL), or the control (1.01±0.3 ng/mL; 58.60±9.00 pg/mL; 543.13±62 pg/mL), respectively. Conclusion Although nesfatin-1 and ghrelin are known as adversely affecting the hormones involving the regulation of appetite and food intake, they all increase in depressive patients and are even associated with the severity of the disease. In clinical medicine, the evaluation of the role of nesfatin-1 and ghrelin in endocrine and neu-roendocrine regulation of major metabolic functions is an important key mechanism in solving numerous diseases associated with endocrine and neuroendocrine disturbance. Increased levels of nesfatin-1 and ghrelin may also be important criteria in describing the prognoses of the patients and the effectiveness of the treatments.

The aims of this study were to investigate the impacts of acute aerobic exercise on circulating levels of hormones associated with energy metabolism, namely leptin, nesfatin-1 and irisin, in trained and untrained male subjects and to determine whether the timing of the exercise (i.e. morning or night) amplified these impacts. Thirty trained (19.2±0.7 years) and 30 untrained (19.5±0.6 years) male subjects performed two aerobic running exercises (3 days between tests) to 64-76% of the subjects’ maximal heart rate for about 30 min. Pre- and post-exercise venous blood samples were taken and analysed for leptin, nesfatin-1 and irisin using enzyme-linked immunosorbent assay (ELISA). Paired samples and independent samples t-tests were used to analyse data. Irisin levels increased in all the subjects (p<0.001). In both groups, nesfatin-1 levels increased significantly after the night-time exercise (p<0.05). Importantly, leptin and nesfatin-1 levels varied among the trained and untrained groups: Both leptin and nesfatin-1 levels increased in 4 (13%) and 12 (40%) subjects, respectively, after the morning exercises, and they increased in 9 (30%) and 10 (33%) subjects, respectively, after the night-time exercise. They decreased in 5 (16%) and 7 (23%) subjects, respectively, after the morning exercise and in 6 (20%) and 3 (10%) subjects, respectively, after the night-time exercise. Exercise may result in increased energy consumption by altering irisin levels. However, due to variations among individuals, increasing leptin and nesfatin-1 levels by reducing food intake may not be applicable.

ObjectiveThe aim of this study was to determine and compare the effects of weight loss achieved through orlistat therapy alone or a combination of orlistat and an aerobic exercise training program on aerobic fitness and body composition in obese females.MethodsTwenty-eight obese patients were randomly assigned to receive 12-week treatment with hypocaloric diet–orlistat or diet–orlistat–exercise. Each participant performed an incremental ramp exercise test every 4 weeks to measure aerobic fitness. Fourteen participants performed continuous exercise (approximately 45 minutes per session) at a work rate corresponding to the anaerobic threshold three times per week.ResultsA decrease in the fat mass to body weight ratio of 3.8% (P=0.006) was observed at the end of the 12 weeks in the orlistat group, while a decrease of 9.5% (P=0.001) was seen in the orlistat–exercise group. Maximal exercise capacity increased by 46.5% in the orlistat–exercise group and by 19.5% in the orlistat group.ConclusionWhile orlistat therapy resulted in an improvement in body composition and aerobic fitness at the end of the 12-week period, its combination with exercise training provided improvements in the same parameters within the first 4 weeks of the study. These additional beneficial effects of combining aerobic exercise with orlistat therapy are important with regards to obesity-associated risk factors.

In this study, the effect of low‐dose curcumin on sperm parameters, reproductive hormones, lipid profile, biochemical antioxidant parameters and the histopathological structure of the testis in diabetic male rats were evaluated. In the study, 28 male Wistar albino rats weighing 300–370 g and aged 8–10 weeks were used. Four groups of equal numbers have been created. Diabetes mellitus was induced with 45 mg/kg streptozotocin (STZ) in seven rats. Curcumin was administered to the rats in curcumin and the diabetes + curcumin group by gavage for 15 days at a dose of 10 mg/kg. Then, the rats were sacrificed. Blood samples and testis tissues were obtained, while the rats were under anaesthesia. Glucose, lipid profile, reproductive hormones, sperm parameters, biochemical antioxidant parameters and histopathological examination of the testis were performed. Abnormal sperm ratio, malondialdehyde, glucose, cholesterol, low‐density lipoprotein, and triglyceride levels and caspase‐3 expression were increased in diabetic rats, while the sperm motility and intensity and reduced glutathione, catalase and testosterone levels were decreased. When low‐dose curcumin (10 mg/kg) was administered to diabetic rats, we found that curcumin significantly increased sperm motility and density, and decreased abnormal sperm rate according to the diabetic group. Moreover, curcumin significantly suppressed the lipid profile and increased follicle‐stimulating hormone (FSH) and testosterone levels compared to the diabetic group. On testicular damage and decreased reproductive hormones caused by diabetes, curcumin may have a protective effect with indirect effect of glycaemic control by curcumin.

Statistically significant alterations were detected in the serum and brain levels of these three peptides in both the PTZ-induced chronic epilepsy model and acute seizure model. The results of this study may suggest that the increase in FNDC5/irisin and nesfatin-1 levels, and the decrease in ghrelin levels may contribute to seizure pathophysiology. However, further studies are needed in order to confirm our hypothesis.

This study aimed to investigate the potential effects of acute soccer matches performed in morning, afternoon and at night on both nesfatin-1 and irisin levels in trained subjects. Total of 20 male subjects performed in soccer matches at three different times of day: morning, afternoon, and night. Pre-and post-match venous blood samples were taken, and levels of both nesfatin-1 and irisin were analysed using the enzyme-linked immunosorbent assay (ELISA). Following all matches, the subjects' irisin levels increased significantly in all subjects (p < 0.0001). Nesfatin-1 levels were also increased after the matches; however, the increase was statistically significant for morning (P=0.01) and night-time (p=0.009). The subjects' nesfatin-1 levels did not increase in all subjects and decrease of nesfatin-1 levels observed in some subjects after matches. This study finds that soccer matches performed different workout times have strong stimulatory effects on irisin levels in all subjects but nesfatin-1 response varied among the subjects and it did not change significantly in afternoon match.

The association between hyperglycaemia and serum nitric oxide (NO) levels has not yet been fully clarified. Thus, it was aimed to evaluate the concentration of NO metabolites (nitrate, nitrite) in diabetic patients and to find the relationship between hyperglycaemia and serum NO levels in diabetic and prediabetic patients, and control groups. In this study, 100 subjects were divided into 3 groups: healthy control (n=20), prediabetic (n=40) and diabetic (n=40). Glycemic control was assessed using glycated hemoglobin (HbA1c). Nitrate and nitrite levels were measured using the Griess reagent. NO was obtained from the sum of nitrates and nitrites. The serum NO level was higher in diabetic (53.4±2.0 μM) and prediabetic patients (51.6±1.6 μM) as compared to that in the control (45.6±1.2 μM), (p<0.05). The NO level was not significantly different in diabetic and prediabetic patients. Higher levels of serum glucose, insulin and HOMA-IR may be responsible for the activation of endothelial cells to increase NO levels. This study supports the role of insulin resistance in increased NO levels in both diabetic and prediabetic patients.