Effects of an energy drink on myonectin in the liver, kidney and skeletal muscle of exercised rats.

Myonectin is a hormone that is produced mainly by skeletal muscle. We investigated the effects of exercise and energy drink (ED) administration on myonectin expression in skeletal muscle, liver and kidney tissue in rats; myonectin is produced by all three tissues. We used 28 male albino rats in four groups: untreated control (C), exercise (E), energy drink (ED) and exercise + energy drink (E + ED). The E and E + ED groups were exercised using a treadmill for 4 weeks. We also administered 3.5 ml/kg/day ED during week 1, 7 ml/kg/day during week 2 and 10 ml/kg/day during weeks 3 and 4 in the E and E + ED groups. We used ELISA to measure the levels of myonectin in skeletal muscle, liver and kidney tissues. We used immunohistochemical staining to investigate the localization and intensity of myonectin in these tissues. The amount of myonectin in skeletal muscle tissue was increased significantly in all experimental groups compared to group C. The amount of myonectin in the ED group was significantly greater than group E. No significant difference was observed in liver tissue; however, the amount of myonectin in the liver of group C was the greatest among all groups. The amount of myonectin in kidney tissue exhibited no significant difference among groups. Consumption of ED during exercise increased the amount of myonectin in kidney and skeletal muscle tissues and decreased it in liver tissue. We suggest that consumption of ED might adapt metabolism to incresed exercise by controling synthesis of myonectin in liver, kidney and skeletal muscle.

Effects of irisin and exercise on adropin and betatrophin in a new metabolic syndrome model.

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.

Cyberbullying among children and youth in Türkiye: A systematic review and meta-analysis.

PROBLEM: It has been reported in various studies that identifying risk and protective factors and outcomes of cyberbullying perpetration (CP) and cyberbullying victimization (CV) is crucial for educational strategies to fight against cyberbullying. The main purpose of the present study is to conduct a meta-analysis and systematic review to identify which risk and protective factors are more strongly associated with CP/CV and possible consequences of CP/CV among children and youth in Türkiye. ELIGIBILITY CRITERIA: Various databases, including PubMed, Web of Science (WoS), ProQuest, ERIC, SCOPUS, Turkish Psychiatry Index, DergiPark, and National Dissertation/Thesis Center of Türkiye were searched to identify relevant studies. SAMPLE: Fifty-nine studies met the inclusion criteria included in the present study. RESULTS: Results revealed that the strongest risk factor was traditional bullying for CP (r = 0.47, p < .001) and traditional victimization for CV (r = 0.43, p < .001). The strongest protective factor was social skill for CP (r = -0.45, p < .001) and empathy for CV (r = -0.25, p < .001). In addition, involvement in CP behaviors had the strongest effect on negative self-concept (r = 0.28, p < .001), while exposure to CV on anxiety (r = 0.35, p < .001). CONCLUSIONS: Although this study has some limitations, the study's findings are important source of information for many professionals, such as pediatric nurses, school psychological counselors, psychologists, and policymakers to further educational strategies for children and young people in Türkiye. IMPLICATIONS: The study findings would be useful for developing educational programs to strengthen protective factors and reduce risk factors to prevent cyberbullying perpetration behaviors.

Betatrophin, elabela, asprosin, glucagon and subfatin peptides in breast tissue, blood and milk in gestational diabetes.

We investigated the presence of asprosin (ASP), betatrophin, elabela (ELA), glucagon and subfatin (SUB) in the milk of mothers with gestational diabetes mellitus (GDM) and compared their levels with blood levels. We also investigated whether these peptides are synthesized by the breast. We investigated 12 volunteer mothers with GDM and 14 pregnant non-GDM control mothers. The peptides were measured using ELISA and their tissue localization was determined using immunohistochemistry. Breast milk contains ASP, betatrophin, ELA, glucagon and SUB. The amount of the peptides ranged from highest to the lowest in colostrum, transitional milk and mature milk. The amount of peptides in the milk was greater than for blood. The peptides, except for ELA, were increased in milk and blood by GDM. Betatrophin and ELA are synthesized in the connective tissue of the breast. ASP, glucagon and SUB are synthesized in the alveolar tissue of the breast. These peptides in breast milk may contribute to the development of the gastrointestinal tract of newborns and infants.

Interleukin 18, soluble cluster of differentiation 40, platelet factor 4 variant 1, and neutrophil gelatinase-associated lipocalin can be used as biomarkers to aid activity and diagnosis in ocular Behçet's disease.

PURPOSE: The molecules human interleukin (IL-18), the soluble cluster of differentiation (sCD40), platelet factor 4 variant 1 (PF4V1), and neutrophil gelatinase-associated lipocalin (NGAL) are all markers of inflammation in biological systems and are linked to prognosis in several inflammatory diseases as well. Since there is no study in which the above-mentioned molecules are studied together in ocular Behçet's disease (OBD), the aim of this study is to reveal whether these molecules are activity markers in active (OABD) and inactive (OIBD) disease. METHODS: 30 OABD and 30 OIBD and 30 healthy individuals were included in the study. IL-18, sCD40, PF4V1, and NGAL molecules were studied in blood samples by the ELISA method. RESULTS: When OABD and OIBD were compared to healthy individuals, the levels of IL-18, sCD40, PF4V1, and NGAL molecules were found to be statistically significant. These values were even more significantly higher in patients with OABD. CONCLUSION: When ROC values of IL-18, sCD40, PF4V1, and NGAL are evaluated, it is clear that these four molecules can be used as biomarkers to aid activity and diagnosis in OBD.

Effects of vitamin D on apoptosis and betatrophin in the kidney tissue of experimental diabetic rats.

The aim of this study is to investigate the effects of vitD on betatrophin and apoptosis in rat kidney tissue using an experimental diabetes model created with STZ. 41 male Wistar-albino breed rat were assigned to 5 groups, which included 3 groups consisting of 7 animals each and 2 groups consisting of 10 animals each. The control group received no treatments. Single-dose 0.1 M sodium buffer was administered ip to the Buffer group. The VitD group was orally administered 200 IU/day vitD.The Diabetes group was injected ip with single-dose 50 mg/kg STZ by dissolving the material in 0.1 M sodium buffer. Subjects with a glucose level exceeding 250 mg/dl were accepted to be diabetic. The Diabetes + VitD group was injected ip with 50 mg/kg single-dose STZ by dissolving the material in 0.1 M sodium buffer. Once diabetes was established, 200 IU/day vitamin D was administered orally. The histological and biochemical analyses of the Control, Buffer, and Vitamin D groups revealed similar serum TOS and TAS levels, and TUNEL positivity and betatrophin immunoreactivity. While the Diabetes group showed significantly higher TOS levels and TUNEL positivity compared to the Control group, their TAS levels and betatrophin immunoreactivity were significantly reduced. The Diabetes+Vitamin group demonstrated significantly lower TOS levels and TUNEL positivity compared to the Diabetic group, and their TAS levels and betatrophin immunoreactivity increased significantly.In conclusion; experimental diabetes was found to increase TOS and apoptotic cells and decrease TAS and betatrophin levels in kidney tissue in experimental diabetes, and that administering VitD as treatment caused a decrease in TOS and apoptotic cells and an increase in TAS and betatrophin levels. It was concluded that future studies needed to investigate various experimental diabetes times so that the role of diabetes in the pathophysiology of its effect on kidney tissue could be uncovered.

Irisin: a potentially candidate marker for myocardial infarction.

Myocardial infarction (MI) causes energy depletion through imbalance between coronary blood supply and myocardial demand. Irisin produced by the heart reduces ATP production by increasing heat generation. Energy depletion affects irisin concentration in circulation and cardiac tissues, suggesting an association with MI. We examined: (1) irisin expression immunohistochemically in rat heart, skeletal muscle, kidney and liver in isoproterenol (ISO)-induced MI, and (2) serum irisin concentration by ELISA. Rats were randomly allocated into 6 groups (n=6), (i) control, (ii) ISO (1h), (iii) ISO (2h), (iv) ISO (4h), (v) ISO (6h), and (vi) ISO (24h), 200mg ISO in each case. Rats were decapitated and the blood and tissues collected for irisin analysis. Blood was centrifuged at 1792 g for 5 min. Tissues were washed with saline and fixed in 10% formalin for histology. Serum irisin levels gradually decreased from 1h to 24h in MI rats compared with controls, the minimum being at 2h, increasing again after 6h. Cardiac muscle cells, glomerular, peritubular renal cortical interstitial cells, hepatocytes and liver sinusoidal cells and perimysium, endomysium and nucleoi of skeletal muscle were irisin positive, but its synthesis decreased 1-4h after MI. At all time-points, irisin increased near myocardial connective tissue, with production in skeletal muscle, liver and kidney recovering after 6h, although slower than controls. Unique insight into the pathogenesis of MI is shown, and the gradually decrease of serum irisin might be a diagnostic marker for MI.