Diabetic bladder dysfunction is associated with bladder inflammation triggered through hyperglycemia, not polyuria

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2018-11-16

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Abstract

Purpose

Diabetes is a grave and progressive condition characterized by debilitating complications. Diabetic bladder dysfunction (DBD) is a very common complication with no specific treatments currently available. Unlike other tissues affected by this disease, the bladder is subjected to two independent insults; 1) polyuria, created by the osmotic effects of glucose in the urine, and 2) hyperglycemia itself. Based on our understanding of inflammation as a major contributor to the underlying organ damage in several other diabetic complications, its presence in the bladder during DBD and the contribution of polyuria and hyperglycemia to its development were assessed.

Methods

Awake, restrained cystometry was performed on wild type C57BL/6 mice and diabetic (Akita) mice on a C57BL/6 background at 15 weeks of age. A subgroup of the Akita mice were treated with phlorizin, an inhibitor of sodium-glucose linked transporter types 1 and 2 that prevents glucose reabsorption in the kidney. All groups were assessed for serum glucose, 4-hour voiding totals, and inflammation in the bladder (Evans blue assay).

Results

Akita mice develop cystometrically-defined DBD by 15 weeks of age, as evidenced by an increase in urinary frequency, a decrease in voiding volume, and an increase in post-voiding residual volume. Phlorizin effectively normalized serum glucose in these animals while increasing the urine output. Inflammation in the bladder was present in the diabetic animals at this time point, but not detectable in animals receiving phlorizin.

Conclusion

Inflammation in the bladder of diabetic mice correlates with the development of DBD and is triggered by hyperglycemia, not polyuria.

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10.2147/rru.s177633

Publication Info

Inouye, BM, FM Jr Hughes, H Jin, R Lütolf, KC Potnis, JC Routh, dc Rouse, WC Foo, et al. (2018). Diabetic bladder dysfunction is associated with bladder inflammation triggered through hyperglycemia, not polyuria. Research and Reports in Urology, 10. pp. 219–225. 10.2147/rru.s177633 Retrieved from https://hdl.handle.net/10161/29069.

This is constructed from limited available data and may be imprecise. To cite this article, please review & use the official citation provided by the journal.

Scholars@Duke

Hughes

Monty Hughes

Assistant Professor in Urology

 Dr. Hughes received his Ph.D. from the Medical University of South Carolina and was a post doc at both the University of North Carolina at Chapel Hill and NIH. He then joined the faculty of the University of North Carolina at Charlotte where he rose to the rank of Associate Professor (with tenure). Following a brief stint as the director of the biology division of a start-up pharmaceutical company, he joined forces with Dr. Purves at the Medical University of South Carolina to begin this lab focused on benign urinary disorders. Dr. Hughes has been at Duke since 2015. He is currently an Assistant Professor working within the Department of Surgery and Division of Urology. He serves as the Director of the Urinary Dysfunction Laboratory which studies the role of inflammation in disorders such as bladder outlet obstruction and diabetic bladder dysfunction. In association with Dr. J Todd Purves, this lab has been instrumental in demonstrating the central importance of the NLRP3 inflammasome in sensing the biochemical stressors associated with these disorders and translating them into an inflammatory signal. This signal is ultimately responsible for changes in voiding function, denervation and fibrosis.

Routh

Jonathan Charles Routh

Paul H. Sherman, M.D. Distinguished Associate Professor of Surgery

I am a pediatric urologist and health services researcher who is interested in caring for children with urological problems, conducting research on how to improve that care, and mentoring young researchers to ensure that the next generation does both better than I currently can. 

My clinical interests include minimally-invasive surgery, neurogenic and non-neurogenic voiding dysfunction, complex urologic reconstruction (particularly in children with spina bifida), and pediatric urologic oncology (particularly Wilms tumor and rhabdomyosarcoma). My research has been funded by awards from the NIH, CDC, FDA, and multiple foundations and industry partners, and during my time on faculty at Duke I have had the pleasure of collaborating with many groups and individuals around the world on a number of projects. Over the past 15 years, I have formally mentored nearly 3 dozen undergraduates, medical students, urology residents, post-doctoral students, and junior faculty members across multiple disciplines (pediatrics, urogynecology, urology, and nursing).

Foo

Wen Chi Foo

Associate Professor of Pathology
Purves

J Todd Purves

Professor of Urology

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