Johanne H Ellenbroek1, Ebru Arioglu Inan2, Martin C Michel3. 1. Department of Internal Medicine, Leiden University Medical Centre, Leiden, The Netherlands. 2. Department of Pharmacology, Ankara University, Ankara, Turkey. 3. Department of Pharmacology, Johannes Gutenberg University, Mainz, Germany.
Abstract
AIMS: To explore whether the bladder hypertrophy consistently seen in rats upon streptozotocin injection also occurs in other animal models of type 1 or 2 diabetes and how hypertrophy is linked to functional alterations of the urinary bladder. 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: Models other than streptozotocin-injected rats and female animals have been poorly studied. Most animal models of diabetes exhibit less bladder hypertrophy as compared to streptozotocin-injected rats. However, this is not linked to type 1 versus 2 diabetes models, and type 2 models with comparable elevation of blood glucose may exhibit strong or only minor hypertrophy. Bladder dysfunction is frequently observed in experimental diabetes and mostly manifests as increased compliance but does not segregate with hypertrophy. It may at least partly reflect the need to handle large amounts of urine in models associated with major elevation of blood glucose. CONCLUSIONS: To better understand the relevance of bladder hypertrophy in many models of experimental diabetes, more studies in models of type 2 diabetes are urgently needed. Moreover, the role of factors other than hypertrophy in the genesis of bladder dysfunction requires further exploration.
AIMS: To explore whether the bladder hypertrophy consistently seen in rats upon streptozotocin injection also occurs in other animal models of type 1 or 2 diabetes and how hypertrophy is linked to functional alterations of the urinary bladder. 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: Models other than streptozotocin-injected rats and female animals have been poorly studied. Most animal models of diabetes exhibit less bladder hypertrophy as compared to streptozotocin-injected rats. However, this is not linked to type 1 versus 2 diabetes models, and type 2 models with comparable elevation of blood glucose may exhibit strong or only minor hypertrophy. Bladder dysfunction is frequently observed in experimental diabetes and mostly manifests as increased compliance but does not segregate with hypertrophy. It may at least partly reflect the need to handle large amounts of urine in models associated with major elevation of blood glucose. CONCLUSIONS: To better understand the relevance of bladder hypertrophy in many models of experimental diabetes, more studies in models of type 2 diabetes are urgently needed. Moreover, the role of factors other than hypertrophy in the genesis of bladder dysfunction requires further exploration.
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