Lean vs. Obese Mice: The Ventral Prostate Revisited

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Fabiane Ferreira Martins; Mariano del Sol ; Marcia Barbosa Aguila & Carlos Alberto Mandarim-de-Lacerda


Obese mice (C57BL/6J-ob/ob) do not express leptin and develops hyperphagia, decreased energy expenditure, obesity, hyperglycemia, hyperinsulinemia, hypothermia, and infertility. Obesity causes reproductive dysfunction with negative impacts on prostatic structure and fertility. We aimed to compare the structure and molecular aspects of the ventral prostate between of lean and obese (ob/ob) mice. Three months old male lean and obese mice had their prostates dissected and prepared for light microscopy and immunofluorescence. In comparison to the lean mouse, the obese mouse showed a substantial structural modification in the ventral prostate starting with an atrophy of the prostate ventral lobe. Histologically, the acini showed a reduction in size, and in the lumen, we found a mixed secretion PAS positive and negative. Epithelial changes consisted of a hypertrophied acinar epithelium with intraepithelial neoplasia focuses. Also, we observed a marked expression of PCNA and Caspase3 in the epithelium indicating even cellular proliferation as cell death. The stroma showed a high activity of the extracellular matrix remodeling with marked deposition of collagen fibers and smooth muscle cells. Around the ventral region, we observed an increase in the presence of adipose tissue. The expressions of interleukin 6 and tumor necrosis factor alpha were present in the ventral prostate of the obese mice indicating inflammation. In conclusion, obesity negatively modulates prostate in ob/ob mice, directly affecting cellular and structural mechanisms necessary for the maintenance of prostate and reproductive structure.

KEY WORDS: Collagen; IL6; TNFalpha, alpha-actin; Reproduction; ob/ob mouse.

How to cite this article

MARTINS, F. F.; DEL SOL, M.; AGUILA, B. M & MANDARIM-DE-LACERDA, C. A. Lean vs. obese mice: The ventral prostate revisited. Int. J. Morphol., 35(2):403-412, 2017.