Bladder Dysfunction in Rats With Metabolic Syndrome Induced by Long-Term Fructose Feeding

Lee, Wei‐Chia; Chien, Chiang Ting; Yu, Hong‐Jeng; Lee, Shih Wei

doi:10.1016/j.juro.2008.01.086

Cited by 57 publications

(63 citation statements)

References 20 publications

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“…Associations between intensity of male LUTS and presence of the metabolic syndrome were also observed from the Boston Area Community Health (BACH) Survey (Kupelian et al 2009). In line with these clinical findings, bladder dysfunction has also been reported in rat models of metabolic syndrome (Chung et al 2013;Lee et al 2008). In line with others (Bunn et al 2015;Kirby et al 2010), we conclude that metabolic syndrome apparently exhibits a more robust association with LUTS than its individual components of dyslipidemia and diabetes.…”

Section: Clinical Associations Between Atherosclerosis Risk Factors Asupporting

confidence: 54%

Are blood vessels a target to treat lower urinary tract dysfunction?

Michel

Chess-Williams

Hegde

2015

Naunyn-Schmiedeberg's Arch Pharmacol

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Bladder dysfunction is common in the general population (Stewart et al. 2010) and even more so among patients seeing a physician for any reason (Goepel et al. 2002). It often manifests as lower urinary tract symptoms (LUTS), a term originally coined to describe voiding and storage symptoms in men with benign prostatic hyperplasia (BPH) but now more universally used to describe any type of voiding and storage symptoms in both sexes. Studies into possible causes of urinary bladder dysfunction have long focused on detrusor smooth muscle cells (Turner and Brading 1999). More recently, it became clear that several other types of cells and organs contribute to regulating detrusor smooth muscle function. These include the urothelium (Andersson and McCloskey 2014; Michel 2015), afferent nerves (Michel and Igawa 2015; Yoshimura et al. 2014b), and the central and autonomic nervous systems (Fowler and Griffiths 2010; Yoshimura et al. 2014a). Alterations in any of these may at least partly be responsible for detrusor dysfunction and, accordingly, be potential targets for the treatment of bladder dysfunction. As highlighted by an article in this issue of Naunyn-Schmiedeberg's Archives of Pharmacology (Bayrak et al. 2015), there is an additional suspect, the bladder vasculature. This article will discuss the currently available experimental and clinical evidence for a role of the vasculature in causing bladder dysfunction, and how existing and emerging treatments may modulate bladder function by acting on blood vessels. Due to a similarity in concept, data on prostate perfusion will also be discussed to some extent.

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Section: Clinical Associations Between Atherosclerosis Risk Factors Asupporting

confidence: 54%

Are blood vessels a target to treat lower urinary tract dysfunction?

Michel

Chess-Williams

Hegde

2015

Naunyn-Schmiedeberg's Arch Pharmacol

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“…This may be another molecular base of OAB in MtS, in rats. Lee et al showed structural changes of cells, in MtS, in another experimental study [21]. In a recent study, Millagro et al reported genetic and molecular base of MtS in women with MtS [22].…”

Section: Discussionmentioning

confidence: 95%

“…It has been accepted that MtS occurs on the basis of insulin resistance (IR) [4]. Thus, endothelial injury may come into question, and this may lead to atherosclerosis which may cause to decrease blood supply of bladder.…”

Section: Introductionmentioning

confidence: 99%

“…Thus, endothelial injury may come into question, and this may lead to atherosclerosis which may cause to decrease blood supply of bladder. At the end of these processes, as a result, LUTS may come into question, which could be showed in experimental studies [4]. However, the accurate cascade of pathophysiology which is ended as LUTS including IR and develop-1 3 ment of atherosclerosis has not been clarified in humans, yet.…”

Section: Introductionmentioning

confidence: 99%

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Relationship between neck circumference and overactive bladder in women with metabolic syndrome: a preliminary study

Akın

Gulmez

Savaş

et al. 2015

Wien Klin Wochenschr

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“…Functionally, there was less contractile activity of the bladder strip to potassium chloride (KCl) in vitro. 25 The authors of the study also observed that mitochondria in bladder smooth muscle cell were denatured , which lead to the idea that oxidative stress existed. These notions support our hypothesis that oxidation-dependent AGE was accumulated in bladder with oxidative stress, which leads inflammatory cells infiltration and accelerates bladder dysfunction.…”

Section: Discussionmentioning

confidence: 97%

Immunohistochemical detection of advanced glycation end products in human bladder with specific monoclonal antibody

Matsumoto¹,

Fujiwara²,

Nagai³

et al. 2009

Int J of Urology

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Objective:To investigate the accumulation of advanced glycation end products (AGE) in human bladder. Methods: Human bladder specimens were obtained from nine patients during radical cystectomy. Frozen sections were immunohistochemically analyzed by three different monoclonal anti-AGE antibodies such as anti-N e -(carboxymethyl)lysine (CML), anti-imidazolone and anti-pentosidine antibodies. Bladder sections were stained with these antibodies by indirect immunoperoxidase methods. Double immunohistochemical staining with one of the anti-AGE antibodies or an anti-human macrophage antibody was also carried out. Results: We demonstrated that CML and pentosidine were accumulated in human bladder extracellularly as well as intracellularly, whereas any accumulation of imidazolone was not observed. Double immunohistochemical staining indicated that AGE-accumulated cells in human bladder were derived from macrophages. Conclusions:The present study demonstrated that AGE-structures such as CML and pentosidine are accumulated extracellularly in human bladder, and were endocytosed by tissue macrophages.

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Bladder Dysfunction in Rats With Metabolic Syndrome Induced by Long-Term Fructose Feeding

Cited by 57 publications

References 20 publications

Are blood vessels a target to treat lower urinary tract dysfunction?

Are blood vessels a target to treat lower urinary tract dysfunction?

Relationship between neck circumference and overactive bladder in women with metabolic syndrome: a preliminary study

Immunohistochemical detection of advanced glycation end products in human bladder with specific monoclonal antibody

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