Laboratory of Medical Research - LIM 55, Urology, University of Sao Paulo Medical School, Sao Paulo, Brazil.
School of Physical Education and Sport, University of Sao Paulo, São Paulo, Brazil.
Physiol Rep. 2021 Apr;9(7):e14792. doi: 10.14814/phy2.14792.
To investigate the role of physical activity in functional and molecular bladder alterations in an obese and insulin-resistant murine model.
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.
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.
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.
研究体力活动在肥胖和胰岛素抵抗的小鼠模型中对功能性和分子膀胱改变的作用。
将 Wistar 大鼠随机分为 1. 体力活动和标准饮食;2. 体力活动和高脂肪饮食;3. 无体力活动和标准饮食;4. 无体力活动和高脂肪饮食。第 1 组和第 2 组进行为期 10 周的游泳训练。进行尿动力学研究(UDS),并使用定量实时聚合酶链反应评估与胰岛素途径相关的膀胱组织基因(IRS1/IRS2/PI3K/AKT/eNOS)的表达。
第 1 组和第 2 组的体重增加量低于第 3 组(213.89±13.77 与 261.63±34.20 克(g),p=0.04)和第 4 组(209.84±27.40 与 257.57±32.95 g,p=0.04)。第 4 组的胰岛素水平更高(6.05±1.79 与 4.14±1.14 ng/ml,p=0.038),胰岛素抵抗的稳态模型评估(HOMA-IR)指数更高(1.95±0.73 与 1.09±0.37,p=0.006)高于第 1 组。在 UDS 上,第 4 组的排尿次数更多(13.6±4.21 与 6.0±1.82,p=0.04),排尿后压力更高(8.06±2.24 与 5.08±1.23,p=0.04),容量更小(0.29±0.18 与 0.91±0.41 ml,p=0.008),膀胱顺应性更低(0.027±0.014 与 0.091±0.034 ml/mmHg,p=0.016)与第 1 组相比。高脂肪饮食与胰岛素信号通路的表达不足有关,而体力活动与通路的过表达有关。
胰岛素信号通路可能参与与高脂肪饮食相关的膀胱功能障碍的发病机制。体力活动可能通过胰岛素途径有助于预防高脂肪饮食引起的膀胱功能障碍。