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|Authors:||Yesilyurt, Zeynep E.|
Castañeda, Tamara R.
Beltran-Ornelas, Jesus H.
Silvia-Velasco, Diana L.
Michel, Martin C.
|Title:||Analysis of 16 studies in nine rodent models does not support the hypothesis that diabetic polyuria is a main reason of urinary bladder enlargement|
|Online publication date:||20-Jan-2023|
|Year of first publication:||2022|
|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 (r2 of pooled data from all studies 0.0621). Insulin levels also failed to correlate to a meaningful extent. Various diets and medications (elafibranor, empagliflozin, linagliptin, semaglutide) had heterogeneous effects on bladder weight that often did not match their effects on glucose levels. We conclude that the presence and extent of bladder enlargement vary markedly across diabetes models, particularly type 2 diabetes models; our data do not support the idea that bladder enlargement is primarily driven by glucose levels/glucosuria.|
610 Medical sciences
|Institution:||Johannes Gutenberg-Universität Mainz|
|Department:||FB 04 Medizin|
|Document type specification:||Scientific article|
|Information on rights of use:||https://creativecommons.org/licenses/by/4.0/|
|Journal:||Frontiers in physiology|
|Pages or article number:||923555|
|Publisher:||Frontiers Research Foundation|
|Appears in collections:||DFG-491381577-G|
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