Lower urinary tract symptoms (LUTS) including overactive bladder, incontinence and flaccid bladder may be the most common complication for patients with diabetes, affecting up to 80–90% of patients by some estimates. We wanted to know which of the mouse strains with high blood glucose would develop bladder symptoms such as those experienced by patients. We therefore used the void spot assay to record how urination in these strains changed over time.
In one study we tested Akita mice which have type I diabetes due to a mutation in the insulin 2 gene. We also tested mice on high fat diets and ob/ob mice which have a leptin mutation and are extremely obese.
Akita males appeared to be a good model for polyuria-related bladder remodeling (large urine volumes), while ob/ob females became somewhat incontinent, in a setting of type 2 diabetes complicated by obesity
In a second study we tested for diabetic bladder dysfunction in three mouse models of type 2 diabetes. These were TallyHo, NoncNZO and KK-Ay mice. We performed periodic assessments of blood glucose, glucose tolerance and micturition (void spot assay) for eight to twelve months in both male and female mice.
Despite all three strains exhibiting high blood glucose, the results of voiding assays were very different among the three. Only male mice of the KK-Ay strain exhibited signs of classic diabetic bladder dysfunction and thus would appear to be one of the most useful models for studying this problem. This study appeared in the journal Metabolites
Other Studies:
Role of NADPH oxidase (NOX) in diabetic bladder dysfunction
Smooth muscle insulin receptor deletion causes voiding dysfunction