OBJECTIVE: To assess fibroblast growth factor-2 (FGF2/bFGF), which is important in the development and maintenance of the normal prostate and in the development of human benign prostatic hyperplasia (BPH) and prostatic carcinoma, in an animal model of experimentally induced diabetes. Materials and methods Using Western blotting and immunohistochemical analyses, the expression of FGF2 in prostates from several groups of rats was investigated. Rats had diabetes for 8 or 16 weeks (induced by intravenous injection with 65 mg/kg streptozotocin); rats were also treated with insulin (starting 8 weeks after the induction of diabetes, for 8 weeks), and two further groups acted as age-matched control rats. Immunohistochemical markers for smooth muscle (alpha-actin) and epithelium (cytokeratin) were used to distinguish different cell types in adjacent prostatic sections. RESULTS: Diabetic rats had smaller prostates and lower serum testosterone levels than their controls; insulin treatment of diabetic rats increased prostatic size and testosterone levels. As shown by Western blotting, diabetes caused greater FGF2 expression than in controls, whereas reverse-transcriptase polymerase chain reaction studies showed similar levels of prostatic FGF-2 mRNA in all groups. Immuno-histochemical studies showed that FGF-2 was expressed in both stromal and epithelial components of the rat prostate. Furthermore, although the expression of FGF2 was higher in epithelial than stromal cells in control prostates, it was distributed uniformly in the diabetic prostate. CONCLUSION: The differences in the level of expression and pattern of distribution of FGF2 suggests a potential role for FGF2 in the changes observed in prostatic growth in diabetic rats.
OBJECTIVE: To assess fibroblast growth factor-2 (FGF2/bFGF), which is important in the development and maintenance of the normal prostate and in the development of humanbenign prostatic hyperplasia (BPH) and prostatic carcinoma, in an animal model of experimentally induced diabetes. Materials and methods Using Western blotting and immunohistochemical analyses, the expression of FGF2 in prostates from several groups of rats was investigated. Rats had diabetes for 8 or 16 weeks (induced by intravenous injection with 65 mg/kg streptozotocin); rats were also treated with insulin (starting 8 weeks after the induction of diabetes, for 8 weeks), and two further groups acted as age-matched control rats. Immunohistochemical markers for smooth muscle (alpha-actin) and epithelium (cytokeratin) were used to distinguish different cell types in adjacent prostatic sections. RESULTS:Diabeticrats had smaller prostates and lower serum testosterone levels than their controls; insulin treatment of diabeticrats increased prostatic size and testosterone levels. As shown by Western blotting, diabetes caused greater FGF2 expression than in controls, whereas reverse-transcriptase polymerase chain reaction studies showed similar levels of prostatic FGF-2 mRNA in all groups. Immuno-histochemical studies showed that FGF-2 was expressed in both stromal and epithelial components of the rat prostate. Furthermore, although the expression of FGF2 was higher in epithelial than stromal cells in control prostates, it was distributed uniformly in the diabetic prostate. CONCLUSION: The differences in the level of expression and pattern of distribution of FGF2 suggests a potential role for FGF2 in the changes observed in prostatic growth in diabeticrats.