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Succinate decreases bladder function in a rat model associated with metabolic syndrome
Monica Velasquez Flores1,2, Abubakr H Mossa1,2, Philippe Cammisotto2
1Division of Urology, Department of Surgery, McGill University, Montreal, Quebec, Canada.
Neurourology and Urodynamics
|April 19, 2018
Summary
Elevated succinate levels impair bladder function, especially in metabolic syndrome. This occurs via the GPR91 receptor, leading to reduced bladder capacity and altered nerve profiles.
Area of Science:
- Metabolic Physiology
- Urology
- Pharmacology
Background:
- Succinate and its receptor GPR91 are linked to metabolic syndrome.
- GPR91 is present in the urinary bladder, suggesting a potential role in bladder function.
Purpose of the Study:
- To investigate the impact of chronically elevated succinate on bladder function.
- To explore the role of GPR91 in succinate-induced bladder dysfunction.
Main Methods:
- Administered daily succinate injections to Sprague-Dawley and Dahl rats for 4 weeks.
- Assessed bladder function using conscious cystometry, contractility studies, and morphological analysis.
- Utilized two-way ANOVA and t-tests for statistical comparisons.
Main Results:
- Dahl rats exhibited inherent bladder dysfunction compared to SD rats.
- Succinate treatment reduced bladder capacity and increased urinary succinate levels.
- Succinate altered bladder collagen, GPR91 expression, and nerve profiles, with reduced contractility in Dahl rats.
Conclusions:
- Succinate negatively impacts bladder function, mediated by GPR91.
- Metabolic disturbances exacerbate succinate's detrimental effects on the bladder.
- Findings enhance understanding of bladder dysfunction in metabolic syndrome.
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