Unveiling the bladder's early response to acute glucosuria: first evidence from an animal study

While chronic damage to the lower urinary tract in diabetic patients is well-known, the specific effects of acute glucosuria on the bladder remain unclear. This study, being the first of its kind in the available literature, aims to exclusively investigate the early effects of acute glucosuria on bladder function and morphology, independent of the broader impacts of diabetes.

Wistar Albino rats were divided into four groups: CONTROL, Empagliflozin (EMPA), Diabetes Mellitus + Empagliflozin (DM + EMPA), and DM. Acute glucosuria was induced using empagliflozin in the EMPA and DM + EMPA groups. The effects on bladder function were assessed through contraction protocols using potassium chloride (KCl), cumulative acetylcholine (ACh) applications and electrical field stimulation studies (EFS). The bladder tissues were also examined histopathologically to evaluate morphological changes.

In the organ bath studies, a significant increase in the response to KCl was observed in the diabetic group receiving empagliflozin compared to others (p < 0.001). When examining the contraction responses to ACh, it was found that the diabetic group receiving empagliflozin exhibited significantly higher contraction responses (p < 0.001). In the EFS, no significant difference was found between the groups. The histopathological examinations revealed a significant muscularis propria hypertrophy in the groups receiving empagliflozin compared to the control group (p < 0.001).

In our study, we found that short-term treatment defined as 15 days with empagliflozin increased the receptor-independent contractile capacity of the bladders in diabetic rats and enhanced their contraction responses to ACh. However, there was no significant difference observed in the EFS studies. Histopathological analysis revealed the development of detrusor hypertrophy in rats receiving empagliflozin treatment.