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Metabolic syndrome decreases tissue perfusion and induces glandular hyperplasia in the fructose‐fed rat prostate
Author(s) -
Chen IHung,
Tong YatChing,
Cheng JueiTang
Publication year - 2012
Publication title -
neurourology and urodynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 90
eISSN - 1520-6777
pISSN - 0733-2467
DOI - 10.1002/nau.21192
Subject(s) - medicine , prostate , hyperplasia , perfusion , metabolic syndrome , endocrinology , blood flow , urology , blood pressure , obesity , cancer
Aims The effects of metabolic syndrome on the prostate blood perfusion and histological structure were studied using fructose‐fed rats (FR). Methods Age‐matched male Wistar rats were divided into two groups: group I, normal control rats and group II, 9‐week FR. Animal body weight, blood pressure, and serum metabolic parameters were monitored. With the rats under anesthesia, prostatic blood flow volume and flow velocity were measured by laser Doppler flowmetry. The prostate was then removed for histological examination and morphometric study. Results The 9‐week FR showed significant increases in body weight, blood pressure, plasma glucose, insulin, and triglyceride levels. The blood flow volume (345.8 ± 20.57 ml/min/100 g vs. 440.4 ± 35.57 ml/min/100 g of tissue, P < 0.05 for n = 8) and flow rate (29.4 ± 1.25 units vs. 40.9 ± 2.65 units, P < 0.05 for n = 8) in the FR ventral prostate were significantly decreased when compared to controls. Structurally, the FR prostate weight was significantly higher than that of the controls (612.4 ± 16.9 mg vs. 427.3 ± 6.5 mg, P < 0.05 for n = 8). Prostate histology showed glandular hyperplasia while morphometry showed increased stromal component in the FR. Conclusions Metabolic syndrome in the FR decreases prostatic perfusion and induces prostatic glandular hyperplasia. The findings suggest that chronic ischemia may be a link between metabolic syndrome and prostatic enlargement. Neurourol. Urodynam. 31:600–604, 2012. © 2012 Wiley Periodicals, Inc.