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Am J Physiol Renal Physiol (November 4, 2009). doi:10.1152/ajprenal.00309.2009
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Submitted on June 1, 2009
Revised on September 22, 2009
Accepted on October 29, 2009

Voiding Function in Obese and Type 2 Diabetic Female Rats

Gregory Gasbarro MS1, Dan L Lin2, Drina Vurbic3, Amanda Quisno3, Bruce Kinley3, Firouz Daneshgari4, and Margot S Damaser5*

1 The Cleveland Clinic
2 Louis Stokes Cleveland VA Medical Center, Cleveland
3 Louis Stokes Cleveland Department of Veterans Affairs Medical Center
4 Upstate Medical University
5 Cleveland Clinic

* To whom correspondence should be addressed. E-mail: damasem{at}ccf.org.

Purpose: 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. Materials and Methods: Age-matched female virgin rats were separated into three experimental groups: Zucker lean rats (control; normal diet, n=22), ZDF rats (obese+non-diabetic; low fat diet, n=22) and ZDF rats (obese+diabetic; high fat diet, n=20). Rats were placed on their specified diet for 10 weeks before urodynamic LUT evaluation. A suprapubic catheter was implanted 2 days prior to urodynamic studies. Voiding function was evaluated by cystometry and leak point pressure testing. The bladder, urethra, and vagina were immediately excised for qualitative histological evaluation. Results: Compared to control rats, obese+non-diabetic 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). Leak point pressure studies showed a non-significant decrease in LPP (P = 0.075) and baseline pressure (P = 0.168) in both obese groups compared to control. Histology of the external urethral sphincter in obese rats showed increased fibrosis leading to disruption of the skeletal muscle structure compared to control. Additionally, the bladder wall of the obese+non-diabetic and obese+diabetic rats demonstrated edema and vasculopathy. Conclusions: 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.







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