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A systematic review of urinary bladder hypertrophy in experimental diabetes: Part I. Streptozotocin‐induced rat models
Author(s) -
Arioglu Inan Ebru,
Ellenbroek Johanne H.,
Michel Martin C.
Publication year - 2018
Publication title -
neurourology and urodynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 90
eISSN - 1520-6777
pISSN - 0733-2467
DOI - 10.1002/nau.23490
Subject(s) - muscle hypertrophy , medicine , diabetes mellitus , streptozotocin , renal hypertrophy , endocrinology , urinary bladder , urology , urinary system , diabetic nephropathy
Aims To better understand the genesis and consequences of urinary bladder hypertrophy in animal models of diabetes. This part of a three‐article series will analyze urinary bladder hypertrophy in the diabetes mellitus type 1 model of rats injected with streptozotocin (STZ). Methods A systematic search for the key word combination “diabetes,” “bladder” and “hypertrophy” was performed in PubMed; additional references were identified from reference lists of those publications. All papers were systematically extracted for relevant information. Results A total of 39 studies were identified that quantitatively reported on bladder hypertrophy in rats upon injection of STZ; of which several reported on multiple time points yielding a total of 83 group comparisons. Bladder hypertrophy was found consistently, being fully developed as early as 1 week after STZ injection (bladder weight 188 ± 59% of matched control). Hypertrophy was similar across sexes and STZ doses (35‐40 vs 50‐65 mg/kg) but appeared greater with Wistar rats than other rat strains. The extent of bladder hypertrophy was not correlated to blood glucose concentrations, but normalization of blood glucose concentration by insulin treatment starting early after STZ injection prevented hypertrophy; insulin treatment starting after hypertrophy had established largely reversed it. Conclusions Bladder size approximately doubles after STZ injection in rats; the extent of hypertrophy is not linked to the severity of hyperglycemia but largely reversible by restoration of euglycemia.