Browsing by Subject "Lower urinary tract symptoms"

Now showing 1 - 2 of 2
  • Thumbnail Image
    Item
    Is the Diabetic Bladder a Neurogenic Bladder? Evidence from the Literature
    (Springer, 2014-12) Powell, C.R.; Urology, School of Medicine
    Diabetes can often cause LUTS. This has been called diabetic cystopathy by many authors, but no concise grouping of symptoms for this condition has been agreed upon. The etiology of diabetic cystopathy remains unknown, but evidence from the literature strongly suggests a neurologic etiology as the primary factor, with other factors such as polyuria, damage to muscle from oxidative stress, and urothelial factors possibly contributing. Once a standard definition for diabetic cystopathy can be agreed upon, prospective, longitudinal studies will play a key role in the generation of hypotheses for the causes of diabetic cystopathy. Animal models will help test these hypotheses and possibly provide strategies for prevention.
  • Thumbnail Image
    Item
    Ossabaw Pig Demonstrates Detrusor Fibrosis and Detrusor Underactivity Associated with Oxidative Stress in Metabolic Syndrome
    (American Association for Laboratory Animal Science, 2020-10) Powell, Charles R.; Kim, Albert; Roth, Joshua; Byrd, James P.; Mohammad, Khalid; Khalid, Mouhamad; Alloosh, Mouhamad; Vittal, Ragini; Sturek, Michael; Urology, School of Medicine
    Metabolic Syndrome (MetS) has detrimental effects on the bladder, including detrusor underactivity. The progression and mechanism of disease are poorly understood. A swine model for diabetic bladder dysfunction (DBD) was established because of the pig's human-sized bladder and its ability to develop MetS by dietary modification alone. The hypothesis of this study is that this swine model will demonstrate oxidative stress associated with MetS, which contributes to both bladder fibrosis and detrusor underactivity (DU). Ossabaw pigs underwent dietary modification consisting of a hypercaloric, atherogenic diet for 10 mo to induce MetS, and were compared with a group of control (lean) pigs. Urodynamic studies were performed in both groups to confirm DU. Thiobarbituric acid reactive substances (TBARS) detected in the urine were used to measure oxidative stress activity in the urinary tract, and urinary IL17a was used to detect profibrotic activity. MetS was confirmed by assessing body weight, blood pressure, glucose tolerance, total cholesterol, and triglycerides. The MetS group exhibited an increase in the relative levels of urinary TBARS and IL17a. Bladder pressures at capacity were lower in the MetS group, suggesting DU. Histologic analysis of a cohort of control (lean) and MetS pigs revealed that as compared with the control pigs, the MetS pigs had significantly more collagen in the muscularis layer, but not in the submucosa or mucosa layer. In conclusion, the Ossabaw pig model for diet-induced MetS is associated with oxidative stress and profibrotic activity in the bladder, which results in DU. This has previously been shown in mice and rats, but never in pigs. This novel model will better represent human MetS and DBD because the mechanism and size of the pig bladder more closely resemble that of a human, resulting in a more valid model and facilitating further study into the signaling mechanisms responsible for this impairment.