Voiding function in obese and type 2 diabetic female rats

Gasbarro G, Lin DL, Vurbic D, Quisno A, Kinley B, Daneshgari F, Damaser MS. Voiding function in obese and type 2 diabetic female rats. Am J Physiol Renal Physiol 298: F72-F77, 2010. First published November 4, 2009; doi:10.1152/ajprenal.00309.2009. 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.