ArticleFrontiers in physiology2022
Analysis of 16 studies in nine rodent models does not support the hypothesis that diabetic polyuria is a main reason of urinary bladder enlargement.
Article in Frontiers in physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- βNeurourology and urodynamics · 2025Review
- Methylglyoxal and Advanced Glycation End Products (AGEs): Targets for the Prevention and Treatment of Diabetes-Associated Bladder Dysfunction?Biomedicines · 2024Review
- Project-Based Public-Private Collaborations.Handbook of experimental pharmacology · 2024Review
- A comparison of urinary bladder weight in male and female mice across five models of diabetes and obesity.Frontiers in pharmacology · 2023Article
- Association of diabetes, hypertension, and their combination with basal symptoms and treatment responses in overactive bladder patients.Frontiers in pharmacology · 2023Article
- Sex and Gender Differences in the Pharmacology of the Overactive Urinary Bladder.Handbook of experimental pharmacology · 2023Review
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Authors and funding
15 authors.
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Abstract
The urinary bladder is markedly enlarged in the type 1 diabetes mellitus model of streptozotocin-injected rats, which may contribute to the frequent diabetic uropathy. Much less data exists for models of type 2 diabetes. Diabetic polyuria has been proposed as the pathophysiological mechanism behind bladder enlargement. Therefore, we explored such a relationship across nine distinct rodent models of diabetes including seven models of type 2 diabetes/obesity by collecting data on bladder weight and blood glucose from 16 studies with 2-8 arms each; some studies included arms with various diets and/or pharmacological treatments. Data were analysed for bladder enlargement and for correlations between bladder weight on the one and glucose levels on the other hand. Our data confirm major bladder enlargement in streptozotocin rats and minor if any enlargement in fructose-fed rats, db/db mice and mice on a high-fat diet; enlargement was present in some of five not reported previously models. Bladder weight was correlated with blood glucose as a proxy for diabetic polyuria within some but not other models, but correlations were moderate to weak except for RIP-LCMV mice (
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