Spirulina platensis (SP) rendered the hematological and biochemical indexes as well as antioxidant levels and the histological architecture to normal status in a dose-dependent manner. Accordingly, the current study recommends the use of SP to remedy the toxic effects of HCQ.The glycogen content in muscle of livestock and poultry animals affects the homeostasis of their body, growth performance, and meat quality after slaughter. FOS-like 2, AP-1 transcription factor subunit (FOSL2) was identified as a candidate gene related to muscle glycogen (MG) content in chicken in our previous study, but the role of FOSL2 in the regulation of MG content remains to be elucidated. Differential gene expression analysis and weighted gene coexpression network analysis (WGCNA) were performed on differentially expressed genes (DEGs) in breast muscle tissues from the high-MG-content (HMG) group and low-MG-content (LMG) group of Jingxing yellow chickens. Analysis of the 1,171 DEGs (LMG vs. HMG) identified, besides FOSL2, some additional genes related to MG metabolism pathway, namely PRKAG3, CEBPB, FOXO1, AMPK, and PIK3CB. Additionally, WGCNA revealed that FOSL2, CEBPB, MAP3K14, SLC2A14, PPP2CA, SLC38A2, PPP2R5E, and other genes related to the classical glycogen metabolism in the same coexpressed module are associated with MG content. Also, besides finding that FOSL2 expression is negatively correlated with MG content, a possible interaction between FOSL2 and CEBPB was predicted using the STRING (Search Tool for the Retrieval of Interacting Genes) database. Furthermore, we investigated the effects of lentiviral overexpression of FOSL2 on the regulation of the glycogen content in vitro, and the result indicated that FOSL2 decreases the glycogen content in DF1 cells. Collectively, our results confirm that FOSL2 has a key role in the regulation of the MG content in chicken. This finding is helpful to understand the mechanism of MG metabolism regulation in chicken and provides a new perspective for the production of high-quality broiler and the development of a comprehensive nutritional control strategy.This study aimed to examine which variable, between the peak running velocity determined on the track field (V peak_TF) and critical speed (CS), is the best predictor of the 5-km running performance in recreational runners. Twenty-five males performed three tests to determine the V peak_TF, CS, and 5-km running performance on the track field, with a minimal interval of 48 h between each test. The V peak _TF protocol started with a velocity of 8 km⋅h-1, followed by an increase of 1 km⋅h-1 every 3 min until volitional exhaustion, which was controlled by sound signals, with cones at every 25 m indicating when the participants were required to pass the cone's position to maintain the required velocity. The participants performed three time trials (TTs) (1 2,600 m; 2 1,800 m; and 3 1,000 m) on the same day, with a 30-min rest period to determine the CS through the combinations of three (CS1,2,3) and two TTs (CS1,2, CS1,3, and CS2,3). The 5-km running performance time was recorded to determine the test duration, and the mean velocity (MV) was calculated. There was a significant difference observed between the V peak_TF and the MV 5-km running performance. However, no differences were found between the CS values and the MV 5-km running performance. A correlation was observed between the V peak_TF (R = -0.90), CS1,2,3 (R = -0.95), CS1,3 (R = -0.95), and the 5-km running performance time. Linear regression indicated that the V peak_TF (R 2 = 0.82), CS1,2,3 (R 2 = 0.90), and CS1,3 (R 2 = 0.90) significantly predicted the 5-km running performance time. The CS results showed a higher predictive power for the 5-km running performance, slightly better than the V peak_TF. Also, CS1,2,3 and the CS1,3 presented the highest predictive power for the 5-km running performance of recreational runners.The role of microRNAs in metabolic diseases has been recognized and modulation of them could be a promising strategy to treat obesity and obesity-related diseases. The major purpose of this study was to test the hypothesis that intramuscular miR-1 precursor replacement therapy could improve metabolic parameters of mice fed a high-fat diet. To this end, we first injected miR-1 precursor intramuscularly in high-fat diet-fed mice and evaluated glucose tolerance, insulin sensitivity, and adiposity. miR-1-treated mice did not lose weight but had improved insulin sensitivity measured by insulin tolerance test. Next, using an in vitro model of insulin resistance by treating C2C12 cells with palmitic acid (PA), we overexpressed miR-1 and measured p-Akt content and the transcription levels of a protein related to fatty acid oxidation.  https://www.selleckchem.com/products/larotrectinib.html  We found that miR-1 could not restore insulin sensitivity in C2C12 cells, as indicated by p-Akt levels and that miR-1 increased expression of Pgc1a and Cpt1b in PA-treated cells, suggesting a possible role of miR-1 in mitochondrial respiration. Finally, we analyzed mitochondrial oxygen consumption in primary skeletal muscle cells treated with PA and transfected with or without miR-1 mimic. PA-treated cells showed reduced basal respiration, oxygen consumption rate-linked ATP production, maximal and spare capacity, and miR-1 overexpression could prevent impairments in mitochondrial respiration. Our data suggest a role of miR-1 in systemic insulin sensitivity and a new function of miR-1 in regulating mitochondrial respiration in skeletal muscle.Complications generated by hyperglycemia present in diabetes mellitus (DM) have been constantly related to oxidative stress and dysfunction in the mitochondrial electron transport chain (ETC). Sirtuin 3 (SIRT3), which is present in mitochondria, is responsible for regulating several proteins involved in metabolic homeostasis and oxidative stress. Studies have suggested alterations in the expression of SIRT3 in DM. The objective of this study was to evaluate the effects of phenolic compounds in jabuticaba (Plinia trunciflora), a berry native to Brazil, on the activity of mitochondrial ETC complexes, SIRT3 protein expression, and oxidative stress parameters in liver of diabetic rats induced by streptozotocin. After type 1 DM induction (streptozotocin 65 mg/kg), diabetic and healthy rats were treated with jabuticaba peel extract (JPE) by gavage (0.5 g/kg of weight) for 30 days. After treatments, those diabetic rats presented impaired activities of complexes I, II, and III of ETC along with an overexpression of SIRT3.