Purpose Diabetes mellitus (DM) is a metabolic disorder caused by an absolute or relative deficiency of insulin, a debilitating and costly disease with multiple serious complications. Lower urinary tract (LUT) complications are among the most common complications of DM. The most common and bothersome LUT complication of DM is diabetic cystopathy, or diabetic bladder dysfunction (DBD). We reviewed the current translational knowledge of DBD. Materials and Methods We performed a search of the English literature through PUBMED. The key words used were “diabetes” and “bladder dysfunction” or “cystopathy”. Our data and perspective are provided for consideration of future direction of research. Results Despite traditional recognition of DBD, as a voiding problem, characterized by poor emptying and overflow incontinence, recent clinical and experimental evidence indicate a presence of storage problems such as urgency, and urge incontinence in DM. Recent experimental evidence from studies of DBD on small animal models of DM, indicate the presence of a temporal effect on DBD: Early phase of DM causes compensated bladder function; and late phase of DM causes decompensated bladder function. The ‘temporal theory’ could plausibly provide the scientific road map for correlation between clinical and experimental findings as well as identification of role of mechanisms such as polyuria, hyperglycemia, oxidative stress, autonomic neuropathy and decompensation of contractile apparatus of the bladder in creation of clinical and experimental manifestations of the DBD. Conclusions DBD includes time-dependent manifestations of storage and emptying problems. Identification of mechanistic pathways would lead us to identification of therapeutic intervention.

Diabetic bladders may undergo a transition from a compensated to a decompensated state and transition in the streptozotocin rat model may begin 9 to 12 weeks after induction.

Mid urethral slings result in bothersome complications which should not be minimized. Awareness of these complications should encourage improvements in patient counseling as well as further investigation of the underlying mechanisms. Decreasing complications should be considered an important outcome for future clinical studies of mid urethral slings.

Diabetic bladder dysfunction is a common complication of diabetes mellitus (DM) with poorly understood natural history. This study examined the temporal changes in bladder function 3, 9, 12, and 20 wk after induction of DM by streptozotocin (STZ) in male C57BL/6 mice compared with that in age-matched diabetic mice treated with insulin, 5% sucrose-induced diuretic mice, and sham-treated control mice. Conscious cystometrograms of mice were examined in addition to the measurements of micturition cycle. Diabetes resulted in decreased body weight. Bladder weight, urine output, bladder capacity, and compliance increased in the DM and diuretic groups. Peak voiding pressure (PVP) increased initially in both DM and diuretic mice. However, in DM mice, PVP dropped dramatically at and after 12 wk. Similar changes in the capacity, compliance, and emptying ability of the bladder were seen during the first 9 wk of the diabetes or diuresis, whereas significant decline in the emptying ability of the bladder was only seen in diabetes after 12 wk of disease in mice. Long-term insulin replacement effectively reversed most changes in bladder function. These results suggest that the transition from a compensated to a decompensated bladder dysfunction occurs 9-12 wk after induction of DM in mice by STZ.

Diabetic bladder dysfunction (DBD) is among the most common and bothersome complications of diabetes mellitus. Autonomic neuropathy has been counted as the cause of DBD. In the present study, we compared the alterations in the neurogenically mediated contractile responses of urinary bladder in rats with streptozocin-induced diabetes, 5% sucrose-induced diuresis, and age-matched controls. Male Sprague-Dawley rats were divided into three groups: 9-wk diabetic rats, diuretic rats, and age-matched controls. Micturition and morphometric characteristics were evaluated using metabolic cage and gross examination of the bladder. Bladder detrusor muscle strips were exposed to either periodic electrical field stimulation (EFS) or to EFS in the presence of atropine, alpha,beta-methylene adrenasine 5'-triphosphate, or tetrodotoxin. The proportions of cholinergic, purinergic, and residual nonadrenergic-noncholinergic (NANC) components of contractile response were compared among the three groups of animals. Diabetes caused a significant reduction of body weight compared with diuresis and controls, although the bladders of diabetic and diuretic rats weighed more than the controls. Both diabetes and diuresis caused significant increase in fluid intake, urine output, and bladder size. Diabetes and diuresis caused similarly increased response to EFS and reduced response to cholinergic component compared with controls. However, the purinergic response was significantly smaller in diuretic bladder strips compared with controls but not in diabetic rats. A residual NANC of unknown origin increased significantly but differently in diabetics and diuretics compared with controls. In conclusion, neurogenically mediated bladder contraction is altered in the diabetic rat. Diabetic-related changes do not parallel diuretic-induced changes, indicating that the pathogenesis of DBD needs further exploration.