Aim: To establish the features of morphofunctional organization of the rat urinary bladder in modeled hyperglycemia, taking into account the complex of structural-metabolic changes in the organism in the dynamics of its development. Materials and Methods: The work was performed in compliance with the rules of humane treatment in experiments on 80 one-year-old male Wistar rats. Streptozotocin diabetes was modeled in 50 animals by single intraperitoneal administration of streptozotocin with material collection on days 14, 28, 42, 56, and 70 of the experiment. Histological, electron microscopic, biochemical, massometric methods, measurement of consumed water and daily diuresis, morphometric methods, cluster analysis, and statistical methods were applied. Results: Urothelial cells form four clusters with histometric and ultrastructural characteristics. Chronological features of streptozotocin diabetes development were confirmed by blood glucose level, glycosylated hemoglobin content, urine glucose concentration, its pH, massometric indicators of body weight and urinary bladder weight, and volumes of consumed liquid and diuresis. Disruption of structural-functional balance between urothelial cell clusters is detected from day 14 until the end of the experiment. On days 14-28 of streptozotocin diabetes development, compensatory hypertrophy of smooth myocytes of the bladder wall with ultrastructural signs of their functional stress was detected, as well as the first signs of diabetic microangiopathy in the bladder wall. From day 56, generalization of sludge syndrome, dystrophic changes in endotheliocytes, and basement membrane edema are observed. Against the background of pronounced microangiopathy, diuresis and polydipsia decrease, desquamation of urothelial cells intensifies, and dehydration of smooth myocytes and urothelial cells occurs, which is pronounced on day 70 of the experiment. Conclusions: In the dynamics of induced hyperglycemia development, disruption of structural-functional balance between urothelial cell clusters was detected, leading to imbalance between proliferative potentials of basal urothelial cells and integrity of the urothelial cellular barrier, as well as stages of differentiation of intermediate urothelial cells. Diabetic microangiopathy intensifies until day 70 of the experiment. Overall, during this period, diabetic cystopathy remains compensated (percentage of smooth myocyte area is 1.16 times greater than control and percentage of collagen fiber area is 1.23 times less than control).