Voiding function in obese and type 2 diabetic female rats

Gasbarro, Gregory; Lin, Dan; Vurbic, Drina; Quisno, Amanda; Kinley, Bruce; Daneshgari, Firouz; Damaser, Margot S.

doi:10.1152/ajprenal.00309.2009

Cited by 36 publications

(37 citation statements)

References 32 publications

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“…These findings are suggestive of an inflammatory process in the stroma of the bladder in the diabetic state may be related to oxidative stress associated with characteristics complications of diabetes mellitus. The severity of bladder injuries is also correlated to the duration of diabetes as observed in other studies 12,20 . Most studies, however, have not correlated morphological bladder lesions with the duration of diabetes mellitus and urodynamic evaluation.…”

Section: Discussionsupporting

confidence: 68%

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Urethral dysfunction due to alloxan-induced diabetes. Urodynamic and morphological evaluation

Pegorare

Gonçalves²,

Suaid³

et al. 2014

Acta Cir. Bras.

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PURPOSE:To evaluate the effect of short and long term alloxan-induced diabetes on bladder and urethral function of female rats, and also describing its correlated morphological alterations. METHODS:Thirty five female rats were divided into three groups: G1 (n=9), control group; G2 (n=17), six weeks alloxan-induced diabetic rats; G3 (n=9), 20 weeks alloxan-induced diabetic rats. Functional evaluation was performed by cystometry and simultaneous measurements of the urethral pressure during bladder filling and voiding. Morphological evaluation was also performed with measurement of bladder and urethral fibrosis and collagen content and thickness of lamina propria and smooth muscle layers. RESULTS:The peak bladder pressures and contraction amplitudes were decreased in 100% and 47% of the G3 and G2 groups respectively, when compared to control. Bladder overactivity was observed in 53% of the G2 group. CONCLUSION:Alloxan-induced diabetes urethropathty in female rat was associated to bladder morphological alterations as higher thicknesses of it lamina propria, detrusor and adventicea.

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Section: Discussionsupporting

confidence: 68%

“…Gasbarro et al 20 carried out histological analysis of the urethra in rats after six weeks of induction of diabetes and found that the external sphincter showed edema and fibrosis periurethral muscle layer. This infiltration of collagen leads to a sharp discontinuity of the urethral striated muscle structure compared with the control group.…”

Section: Discussionmentioning

confidence: 99%

Urethral dysfunction due to alloxan-induced diabetes. Urodynamic and morphological evaluation

Pegorare

Gonçalves²,

Suaid³

et al. 2014

Acta Cir. Bras.

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“…This is primarily due to the relative ease of inducing type I diabetes in animal models, typically using either alloxan or high doses of STZ, and the lower costs associated with developing and maintaining animals with type I diabetes. Unfortunately, the literature on the effects of type II diabetes on bladder function is sparse (21). Studies determining the time course of diabetic bladder dysfunction in type II diabetic animal models are severely lacking along with studies determining whether bladder dysfunction is similar in type I vs. type II diabetic animal models (13).…”

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confidence: 99%

Effect of type II diabetes on male rat bladder contractility

Kendig

Ets

Moreland

2016

American Journal of Physiology-Renal Physiology

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Kendig DM, Ets HK, Moreland RS. Effect of type II diabetes on male rat bladder contractility. Am J Physiol Renal Physiol 310: F909 -F922, 2016. First published January 28, 2016 doi:10.1152/ajprenal.00511.2015.-Type II diabetes is the most prevalent form of diabetes. One of the primary complications of diabetes that significantly affects quality of life is bladder dysfunction. Many studies on diabetic bladder dysfunction have been performed in models of type I diabetes; however, few have been performed in animal models of type II diabetes. Using the Zucker Diabetic Fatty (ZDF) rat model of type II diabetes, we examined the contractility and sensitivity of bladder smooth muscle in response to mediators of depolarization-induced contraction, muscarinic receptor-mediated contraction, ATP-induced contraction, and neurogenic contraction. Studies were performed at 16 and 27 wk of age to monitor the progression of diabetic bladder dysfunction. Voiding behavior was also quantified. The entire bladder walls of diabetic rats were hypertrophied compared with that of control rats. Contractility and sensitivity to carbachol and ATP were increased at 27 wk in bladder smooth muscle strips from diabetic rats, suggesting a compensated state of diabetic bladder dysfunction. Purinergic signaling was increased in response to exogenous ATP in bladders from diabetic animals; however, the purinergic component of neurogenic contractions was decreased. The purinergic component of neurogenic contraction was reduced by P2X receptor desensitization, but was unchanged by P2X receptor inhibition in diabetic rats. Residual and tetrodotoxin-resistant components of neurogenic contraction were increased in bladder strips from diabetic animals. Overall, our results suggest that in the male ZDF rat model, the bladder reaches the compensated stage of function by 27 wk and has increased responsiveness to ATP. diabetic bladder dysfunction; Zucker diabetic fatty rat; muscarinic receptors; purinergic receptors; electrical field stimulation DIABETES MELLITUS (DM) IS a disorder of carbohydrate metabolism typically characterized by defective insulin secretion or insulin resistance and subsequent hyperglycemia. In the past few decades, the prevalence of DM has been on the rise (1, 33), and lower urinary tract symptoms (LUTS) are among the most common complications of diabetes affecting up to 80% of patients (14). The most common and bothersome LUTS in diabetes is bladder dysfunction, with over 50% of diabetic patients experiencing some form of bladder dysfunction (48). The primary classic symptom diabetic patients exhibit is increased residual urine volume after voiding (23). More recent research suggests a combination of both storage and voiding problems (14). Experimental evidence now suggests a temporal profile of the development of diabetic bladder dysfunction (15). There is a progression from the compensated state, during which the bladder undergoes hypertrophy and the muscle becomes hypercontractile, to the decompensated state, when the muscle is hyp...

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“…Alterations in both urodynamic profile and bladder reactivity in vitro have been described in different animal models of obesity (Rahman et al, 2007;Gasbarro et al, 2010;Lee et al, 2011;Leiria et al, 2012). However, no study has evaluated the potential implications of impairment of USM relaxations contributing to overall obesity-related micturition problems.…”

Section: Discussionmentioning

confidence: 99%

“…The prevalence of OAB and metabolic syndrome in the U.S. adult population is 16% and 26%, respectively (Irwin et al, 2011). Animal models have provided evidence to confirm a relationship between metabolic syndrome/hyperlipidemia and OAB symptoms (Rahman et al, 2007;Nobe et al, 2008;Lee et al, 2011;Gasbarro et al, 2010). Obesity-associated insulin resistance has been shown to play an important role in OAB pathophysiology in mice (Leiria et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Soluble Guanylyl Cyclase (sGC) Degradation and Impairment of Nitric Oxide-Mediated Responses in Urethra from Obese Mice: Reversal by the sGC Activator BAY 60-2770

Alexandre

Leiria

Silva

et al. 2014

J Pharmacol Exp Ther

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Obesity has emerged as a major contributing risk factor for overactive bladder (OAB), but no study examined urethral smooth muscle (USM) dysfunction as a predisposing factor to obesityinduced OAB. This study investigated the USM relaxant machinery in obese mice and whether soluble guanylyl cyclase ( Long-term oral BAY 60-2770 administration fully prevented the impairment of USM relaxations in obese mice. Reactiveoxygen species (ROS) production was enhanced, but protein expression of b1 second guanylate cyclase subunit was reduced in USM from obese mice, both of which were restored by BAY 60-2770 treatment. In conclusion, impaired USM relaxation in obese mice is associated with ROS generation and down-regulation of sGC-cGMP signaling. Prevention of sGC degradation by BAY 60-2770 ameliorates the impairment of urethral relaxations in obese mice.

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Voiding function in obese and type 2 diabetic female rats

Cited by 36 publications

References 32 publications

Urethral dysfunction due to alloxan-induced diabetes. Urodynamic and morphological evaluation

Urethral dysfunction due to alloxan-induced diabetes. Urodynamic and morphological evaluation

Effect of type II diabetes on male rat bladder contractility

Soluble Guanylyl Cyclase (sGC) Degradation and Impairment of Nitric Oxide-Mediated Responses in Urethra from Obese Mice: Reversal by the sGC Activator BAY 60-2770

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