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Physical activity effects on bladder dysfunction in an obese and insulin‐resistant murine model

OBJECTIVE: To investigate the role of physical activity in functional and molecular bladder alterations in an obese and insulin‐resistant murine model. METHODS: Wistar rats were randomized into 1. physical activity and standard diet; 2. physical activity and high‐fat diet; 3. no physical activity an...

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Detalles Bibliográficos
Autores principales: de Oliveira, André Matos, Fonseca, Fernando Mello Froes, Reis, Sabrina Thalita, Viana, Nayara Izabel, Oliveira, Edilamar Menezes, Leiria, Luiz Osório, Leite, Katia Ramos Moreira, Nahas, William Carlos, Srougi, Miguel, Antunes, Alberto Azoubel
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8077148/
https://www.ncbi.nlm.nih.gov/pubmed/33904660
http://dx.doi.org/10.14814/phy2.14792
Descripción
Sumario:OBJECTIVE: To investigate the role of physical activity in functional and molecular bladder alterations in an obese and insulin‐resistant murine model. METHODS: Wistar rats were randomized into 1. physical activity and standard diet; 2. physical activity and high‐fat diet; 3. no physical activity and standard diet; and 4. no physical activity and high‐fat diet. Groups 1 and 2 were subjected to a 10‐week swimming protocol. Urodynamic study (UDS) was performed, and the expression of genes in the bladder tissue related to the insulin pathway (IRS1/IRS2/PI3K/AKT/eNOS) was assessed using quantitative real‐time polymerase chain reaction. RESULTS: Groups 1 and 2 presented lower body weight gains than groups 3 (213.89 ± 13.77 vs 261.63 ± 34.20 grams (g), p = 0.04) and 4 (209.84 ± 27.40 vs 257.57 ± 32.95 g, p = 0.04), respectively. Group 4 had higher insulin level (6.05 ± 1.79 vs 4.14 ± 1.14 ng/ml, p = 0.038) and higher homeostasis model assessment of insulin resistance (HOMA‐IR) index (1.95 ± 0.73 vs 1.09 ± 0.37, p = 0.006) than group 1. On UDS, group 4 had greater number of micturition (13.6 ± 4.21 vs 6.0 ± 1.82, p = 0.04), higher postvoid pressure (8.06 ± 2.24 vs 5.08 ± 1.23, p = 0.04), lower capacity (0.29 ± 0.18 vs 0.91 ± 0.41 ml, p = 0.008), and lower bladder compliance (0.027 ± 0.014 vs 0.091 ± 0.034 ml/mmHg, p = 0.016) versus group 1. High‐fat diet was related to an underexpression throughout insulin signaling pathway, and physical activity was related to an overexpression of the pathway. CONCLUSIONS: The insulin signaling pathway may be involved in the pathogenesis of bladder dysfunction related to a high‐fat diet. Physical activity may help to prevent bladder disfunction induced by a high‐fat diet through the insulin pathway.