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首页> 外文期刊>American Journal of Physiology >Voiding function in obese and type 2 diabetic female rats.
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Voiding function in obese and type 2 diabetic female rats.

机译:肥胖和2型糖尿病雌性大鼠的排尿功能。

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The effects of obesity and type 2 diabetes (DMII) on the lower urinary tract (LUT) were characterized by evaluating voiding function and anatomy in female Zucker diabetic fatty (ZDF) rats. Age-matched female virgin rats were separated into three experimental groups: Zucker lean rats (control; normal diet, n = 22), ZDF rats (obese+nondiabetic; low-fat diet, n = 22), and ZDF rats (obese+diabetic; high-fat diet, n = 20). Rats were placed on their specified diet for 10 wk before urodynamic LUT evaluation. A suprapubic catheter was implanted 2 days before urodynamic studies. Voiding function was evaluated by cystometric and leak point pressure (LPP) testing. The bladder, urethra, and vagina were immediately excised for qualitative histological evaluation. Compared with control rats, obese+nondiabetic and obese+diabetic rats had significantly decreased contraction pressure (P = 0.003) and increased cystometric filling volume (P < 0.001). Both obese groups exhibited significantly higher voided volumes (P = 0.003), less frequent urinary events (P < 0.001), and increased residual volumes (P = 0.039). LPP studies showed a nonsignificant decrease in LPP (P = 0.075) and baseline pressure (P = 0.168) in both obese groups compared with control. Histology of the external urethral sphincter in obese rats showed increased fibrosis, leading to disruption of the skeletal muscle structure compared with control. Additionally, the bladder wall of the obese+nondiabetic and obese+diabetic rats demonstrated edema and vasculopathy. Voiding dysfunction was evident in both obese groups but with no significant differences due to DMII, suggesting that voiding dysfunction in DMII may be attributable at least in part to chronic obesity.
机译:通过评估患者Zucker糖尿病脂肪(ZDF)大鼠的排尿功能和解剖学,表征肥胖症和2型糖尿病(DMII)对低尿路(LUT)的影响。年龄匹配的女性维珍大鼠分为三个实验组:Zucker瘦大鼠(对照;正常饮食,N = 22),ZDF大鼠(肥胖+非脂肪酸;低脂饮食,N = 22)和ZDF大鼠(肥胖+糖尿病;高脂饮食,n = 20)。在尿动力学LUT评估之前,将大鼠置于其特定的饮食中10周。在尿动动力学研究之前植入了一只静冈导管。通过囊曲线和泄漏点压力(LPP)测试评估空隙功能。立即切除膀胱,尿道和阴道进行定性组织学评估。与对照大鼠相比,肥胖+非糖尿病和肥胖+糖尿病大鼠显着降低了收缩压力(P = 0.003)和增加的膀胱液填充体积(P <0.001)。肥胖群体均显示出明显较高的空隙量(P = 0.003),越常尿液事件(P <0.001),并增加残余体积(P = 0.039)。与对照相比,LPP研究表明,在两种肥胖基团中,LPP(P = 0.075)和基线压力(P = 0.168)的显着性降低。肥胖大鼠外尿道括约肌的组织学表现出纤维化增加,导致骨骼肌结构与对照相比的破坏。另外,肥胖+非糖尿病和肥胖+糖尿病大鼠的膀胱壁证明了水肿和血管病变。在肥胖群体中,空隙功能障碍明显明显,但由于DMII没有显着差异,表明DMII中的功能障碍至少部分可归因于慢性肥胖症。

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