Obesity-initiated metabolic syndrome promotes urinary voiding dysfunction in a mouse model

doi:10.1002/pros.23185

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	Obesity-initiated metabolic syndrome promotes urinary voiding dysfunction in a mouse model
	He, QQ; Babcook, MA; Shukla, S; Shankar, E; Wang, ZP; Liu, GM; Erokwu, BO; Flask, CA; Lu, L; Daneshgari, F
刊名	PROSTATE
	2016-08-01
卷号	76 期号:11 页码:964-976
关键词	metabolic syndrome lower urinary tract symptoms overactive bladder prostate hyperplasia urinary incontinence
ISSN号	0270-4137
DOI	10.1002/pros.23185
文献子类	Article
英文摘要	OBJECTIVEAccumulating evidences suggests that obesity and metabolic syndrome (MetS) contribute towards lower urinary tract symptoms (LUTS) through alterations in the phenotype of bladder and prostate gland. Clinical studies indicate a link between MetS and LUTS. Nevertheless, there is lack of suitable animal model(s) which could illustrate an association linking obesity to LUTS. We examined the lower urinary tract function in an obesity-initiated MetS mouse model. METHODSMale C57BL/6N wild-type and obese B6.V-Lepob/J maintained on regular diet for 28weeks were subjected to the assessment of body weight (BW), body length (BL), waist circumference (WC), body mass index (BMI), blood glucose (BG), plasma insulin (INS), plasma leptin (LEP), total cholesterol (CHO), free fatty acid (FFA), and measurement of urinary functions. Whole animal peritoneal and subcutaneous adipose tissue measurements as well as prostate and bladder volumes were analyzed by MRI followed by histological evaluation. These parameters were used to draw correlations between MetS and LUTS. RESULTSObesity parameters such as BW, WC, and BMI were significantly higher in B6.V-Lepob/J mice compared to C57BL/6N mice (P<0.01). Higher levels of total CHO and FFA were noted in B6.V-Lepob/J mice than C57BL/6N mice (P<0.05). These results were concurrent with frequency, lower average urine volume and other urinary voiding dysfunctions in B6.V-Lepob/J mice. MRI assessments demonstrate marked increase in body fat and prostate volume in these mice. Compared to C57BL/6N mice, histological analysis of the prostate from B6.V-Lepob/J mice showed increased proliferation, gland crowding, and infiltration of immune cells in the stroma; whereas the bladder urothelium was slightly thicker and appears more proliferative in these mice. The regression and correlation analysis indicate that peritoneal fat (R=0.853; P<0.02), CHO (R=0.729; P<0.001), BG (R=0.712; P<0.001) and prostate volume (R=0.706; P<0.023) strongly correlate with LUTS whereas BMI, WC, INS, and FFA moderately correlate with the prevalence of bladder dysfunction. CONCLUSIONOur results suggest that LUTS may be attributable in part to obesity and MetS. Validation of an in vivo model may lead to understand the underlying pathophysiological mechanisms of obesity-related LUTS in humans. Prostate 76:964-976, 2016. (c) 2016 Wiley Periodicals, Inc.
学科主题	Endocrinology & Metabolism ; Urology & Nephrology
出版地	HOBOKEN
资助项目	国家留学基金委项目 ; 美国国立卫生研究院项目
项目编号	United States Public Health Services [P20DK090871] ; China Scholarship Council [201306180078]
语种	英语
WOS记录号	WOS:000379169700002
资助机构	CSC ; NIH
内容类型	期刊论文
源URL	[http://ir.lzu.edu.cn/handle/262010/179452]
专题	第二临床医学院_期刊论文
通讯作者	Gupta, S (reprint author), Case Western Reserve Univ, Dept Urol, 10900 Euclid Ave, Cleveland, OH 44106 USA.; Gupta, S (reprint author), Univ Hosp Case Med Ctr, 10900 Euclid Ave, Cleveland, OH 44106 USA.
推荐引用方式 GB/T 7714	He, QQ,Babcook, MA,Shukla, S,et al. Obesity-initiated metabolic syndrome promotes urinary voiding dysfunction in a mouse model[J]. PROSTATE,2016,76(11):964-976.
APA	He, QQ.,Babcook, MA.,Shukla, S.,Shankar, E.,Wang, ZP.,...&Gupta, S .(2016).Obesity-initiated metabolic syndrome promotes urinary voiding dysfunction in a mouse model.PROSTATE,76(11),964-976.
MLA	He, QQ,et al."Obesity-initiated metabolic syndrome promotes urinary voiding dysfunction in a mouse model".PROSTATE 76.11(2016):964-976.