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(1) Background: Obesity is a global epidemic issue that has increased greatly in recent decades. Although interventions such as nutritional approaches and the practice of physical exercise are potential therapies to combat obesity, in some cases they are not sufficient. Therefore, the development of new pharmacological treatments is necessary. Combining these therapies with non-pharmacological alternatives could be an interesting strategy for treating obesity. Considered a pharmacological treatment for overactive bladder (OAB), mirabegron is also categorized as a β(3)-adrenoceptor agonist, and is used in recommended doses of 25 mg and 50 mg. Animal models have shown that the administration of 0.8 mg/kg of mirabegron leads to elevated activation of brown adipose tissue (BAT) and white adipose tissue (WAT) browning. (2) Results: Findings suggest that the pharmacological application of mirabegron has numerous beneficial effects in lipid metabolism, suggesting a potential action against obesity. In this context, physical exercise and mirabegron stimulate browning activation using different mechanisms. (3) Conclusions: According to the results of the studies presented in this review, mirabegron may be a promising pharmacological treatment for obesity due to its significant effects on estimated energy expenditure (EER) through thermogenesis elevation, BAT activation, and WAT browning seen in dosages up to 100 mg. In addition, the administration of mirabegron combined with physical exercise may be a potential alternative for increasing the body’s energy expenditure, with actions in distinct signaling pathways. Thus, physical exercise combined with mirabegron can alleviate some adverse side effects encountered with the use of the medication. Finally, although there have been advances in knowledge, more studies are needed to understand the combined effects of using mirabegron and physical exercise.

The preventive and therapeutic role of physical exercise in Parkinson's disease (PD) has been the target of study of many scientific groups, and the research often is done in experimental models, especially rodents. Thus, the aim of this review was to analyze a database, elucidating the main benefits that the systematized practice of physical activity/ exercises can contribute to PD in animal models. Method: Based on this question, a search on PubMed and Medline database containing the terms: "Parkinson's disease" AND "animal model" AND "physical exercise" was performed. The most pertinent studies were selected by the criteria year of publication (2009-2018) and the original article. It was used papers involving animal models and physical exercises, as well as other studies, which allowed an introductory explanation in PD, covering its pathophysiology, and the neurochemical responses of physical exercise in rodents. Results: The results showed that there was a decrease in the levels of nigrostriatal neurodegeneration and an increase in the neuroprotective effect related to the training program. Conclusion: It was concluded that physical exercise has been pointed as an important neuroprotective strategy in animal models of Parkinson's disease, especially those applied at moderate intensities, which were effective in reducing the inflammatory profile, elevating the expression of genes and proteins related to neuronal restoration, mitochondrial biogenesis, repair of the dopaminergic system, besides other events also capable of reflecting improvements in motor and cognitive behavior of animals.

Notch1 protein has an important role in the hepatic metabolism. In this way, it has been observed in obese individuals that Notch1 is correlated with insulin resistance in the liver, which makes it an interesting research target. On the other hand, the physical exercise are associated with the prevention and treatment of insulin resistance and type 2 diabetes. Thus, the present study aims to verify the role of physical exercise in the Notch1 protein modulation in the hepatic tissue of obese mice and its contribution in the control of gluconeogenesis. For this, we used obese mice induced by high fat diet and ob/ob animals. The trained animals group performed treadmill-running protocol, with intensity corresponding to 70% of the maximum running speed, for a period of four weeks. At the end of the exercise protocol (24 hours later), we analyzed the physiological parameters, mRNA levels, and protein content of key molecules in the control of gluconeogenesis and Notch1 signaling. We found that exercise reversed the physiological damage generated by obesity. In addition, trained animals showed a reduction in protein content and Notch1 activity when compared to the sedentary obese group. Furthermore, we observed reduction in pyruvate intolerance in exercised animals and a decrease in gluconeogenesis enzymes. Such findings were also observed in ob/ob mice submitted to physical exercise. Thus, we verified the physical exercise mice reduce Nocth1 activation and decrease PEPCK protein content. Finally, we found that inhibition of Notch1 activity decreases pyruvate intolerance as well as reduces the protein content of gluconeogenesis enzymes. Therefore, we concluded that physical exercise is able to modulate the Notch1 pathway in the liver and contribute to the gluconeogenesis control in obese mice. Disclosure R.C. Gaspar: None. V. Muñoz: None. S.C. Nakandakari: None. B.M. Crisol: None. R.F.L. Vieira: None. L.R. Conceição: None. A. Silva: None. D.E. Cintra: None. L.P. Moura: None. E.R. Ropelle: None. J.R. Pauli: None. Funding São Paulo Research Foundation (2019/11338-9, 2017/20542-3)

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