Functional and structural alterations in urinary bladder of an obese Zucker rat model

Diabetic bladder dysfunction (DBD) is a most common complication of diabetes mellitus (DM), and is seen in 40–80% of diabetic patients. It is characterized by impaired bladder sensation, increased bladder capacity, decreased bladder contractility and increased residual urine. The goals of these studies were to test the hypothesis that the obese Zucker rat is an appropriate model for type 2 diabetic bladder investigations and to define the alterations in bladder structure and functional responses in this setting. Histological examination of bladder cross sections was shown that total bladder wall thickness and threshold pressure of voiding were significantly increased in obese rats, while voiding time, maximal intravesical pressure and intercontraction intervals significantly declined as compared to age‐matched lean rats, respectively. Contractile responses of obese DM strips to Aceltylchine (Ach) and KCl were significantly less than those of bladder strips from lean animals. In addition to generating less force, it can also be seen that strips from the obese DM strips showed slower rate of force development than strips from lean animals. Two major myosin isofroms, SM1 and SM2 myosin heavy chains (MHCs) were separated, estimated and the ratios averaged shown that the SM2‐to‐SM1 isoform ratios were declined in obese bladders. After 12 % SDS‐PAGE, transfered and immunoreacted with antibody against tropomyosin (Tm) and α‐actin (as an internal control), the Tm/α‐actin ratios increased in obese bladders as compared to age‐matched lean bladders. All the data indicated that the obese Zucker rat is a relevant model for type 2 diabetic bladder investigations than the streptozotocin‐induced animal model.