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

Authors Inouye BM, Hughes FM Jr, Jin H, Lütolf R, Potnis KC, Routh JC, Rouse DC, Foo WC, Purves JT

Received 19 June 2018

Accepted for publication 21 August 2018

Published 16 November 2018 Volume 2018:10 Pages 219—225


Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Dr Jan Colli

Brian M Inouye,1 Francis M Hughes Jr,1,2 Huixia Jin,1 Robin Lütolf,3 Kunal C Potnis,1 Jonathan C Routh,1,4 Douglas C Rouse,5 Wen-Chi Foo,6 J Todd Purves1,2,4

1Department of Surgery, Division of Urology, Duke University Medical Center, Durham, NC, USA; 2Department of Bioengineering, Clemson University, Clemson, SC, USA; 3Department of Health Science and Technology, ETH Zurich, Zürich 8092, Switzerland; 4Department of Pediatrics, Duke University Medical Center, Durham, NC, USA; 5Division of Laboratory Animal Medicine, Duke University Medical Center, Durham, NC, USA; 6Department of Pathology, Duke University Medical Center, Durham, NC, USA

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.

Keywords: diabetes, inflammation, urinary bladder, urodynamics, cystitis, immunity, innate

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