Abstract

maintained on regular diet for 30 weeks. Animals 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 evaluated for urinary voiding functions. Total body fat measurement, prostate and bladder volumes were analyzed by MRI followed by histological evaluation of the organs. These parameters were used to examine the associations between MS and LUTS. RESULTS: Obesity 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 inB6.V-Lepob/Jmice.MRIassessmentdemonstratemarked increase in body fat and prostate volume in these mice. Histology of prostate in B6.V-Lepob/J mice showed increased gland crowding and infiltration of immune cells in the stroma, compared to C57BL/6N mice. The regression and correlation analysis indicate that peritoneal fat (R1⁄40.831; p<0.002), BG (R1⁄40.712; p<0.01) and prostate volume (R1⁄40.706; p<0.05) strongly correlate with LUTS whereas BMI, WC, BMI, INS, CHO and FFA moderately correlate with the prevalence of voiding dysfunctions. CONCLUSIONS: Our findings suggests that LUTS may be attributable in part to obesity and MS. Further examination of our in vivo model may lead to understand the underlying pathophysiological mechanisms of obesity-induced LUTS in humans.

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