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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. [ABSTRACT FROM AUTHOR]

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., İrisin 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. [ABSTRACT FROM AUTHOR]

Exercise training increases fibronectin type III domain-containing protein 5 (FNDC5/irisin) via the peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α)-pathway. The PGC1α pathway induced FNDC5/irisin changes in response to exercise training and ischemic stroke are not entirely understood. We investigated the relation of the PGC-1α/FNDC5/irisin pathway to exercise training and to the pathophysiology of ischemic stroke in paretic muscles of stroke-induced rat models. We induced cerebral ischemia following completion of high-intensity interval training (HIIT) to evaluate PGC1α-pathway biofactors in paretic muscles. To define the underlying molecular mechanisms for improvement in paretic muscles following cerebral ischemia, we evaluated PCG-1α-pathway factors using immunofluorescence tracking and enzyme-linked immunosorbent assay (ELISA) immunoassay. We found that HIIT for 3 weeks produced increased expression and release of PGC-1α-pathway biomarkers in both the serum and paretic muscle of stroke-induced rats. We also found a close relation between the expression of PCG-1α-pathway factors in skeletal muscle and their concentration in blood. We found that PGC-1α-pathway biomarkers cause irisin up-regulation following induction of cerebral ischemia. The reduction in neurofunctional deficits following increased PGC-1α-pathway biomarkers suggests that these factors may act as markers of improvement in paretic muscle healing following cerebral ischemia. [ABSTRACT FROM AUTHOR]

Highlights: [•] Salivary glands, eccrine sweat glands and sebaceous glands in the skin produce irisin. [•] Salivary and serum irisin increased significantly after showering at a Turkish bath. [•] Salivary and serum irisin increased significantly after moderate exercise. [•] Salivary irisin correlated significantly with serum irisin. [•] Salivary and serum irisin correlated significantly with BMI. [ABSTRACT FROM AUTHOR]