Oberbach A, Schlichting N, Heinrich M, Kullnick Y, Lehmann S, Adams V, Stolzenburg J-W, Neuhaus J
Klinik für Herzchirurgie, Herzzentrum Leipzig, Leipzig, Deutschland.
Urologe A. 2014 Dec;53(12):1805-11. doi: 10.1007/s00120-014-3659-1.
Obesity with its multiple comorbidities has become a global pandemia. We here report on the pathophysiological aspects of obesity-associated urinary bladder dysfunctions.
Our results are based on multiple in vitro and in vivo studies including a high fat diet (HFD) rat animal model of which the details are given in the cited publications.
In cultured human detrusor muscle cells, obesity-related pathophysiological mechanisms were directly induced by the saturated free fatty acid palmitate. In HFD animals, we found serious fibrosis of the bladder wall and downregulation of the muscarinic M3-receptor leading to diminished contractility of the urinary bladder. Bariatric surgical intervention (sleeve gastrectomy) reversed the fibrosis.
Our results support the relevance of obesity for urological bladder dysfunction. The epidemic dimension of obesity with its steadily growing number of cases requires a re-evaluation of this pathological condition in the urological context.
肥胖及其多种合并症已成为全球大流行疾病。我们在此报告肥胖相关膀胱功能障碍的病理生理方面。
我们的结果基于多项体外和体内研究，包括高脂肪饮食（HFD）大鼠动物模型，其详细信息在引用的出版物中给出。
在培养的人逼尿肌细胞中，饱和游离脂肪酸棕榈酸直接诱导了与肥胖相关的病理生理机制。在HFD动物中，我们发现膀胱壁严重纤维化，毒蕈碱M3受体下调，导致膀胱收缩力减弱。减重手术干预（袖状胃切除术）逆转了纤维化。
我们的结果支持肥胖与膀胱功能障碍的相关性。肥胖病例数量不断增加的流行趋势要求在泌尿外科背景下重新评估这种病理状况。
