Effects of metformin on prostatic tissue of rats with metabolic syndrome and benign prostatic hyperplasia
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To investigate the efficacy of insulin sensitizer on prostatic tissue in animal model with benign prostatic hyperplasia (BPH) secondary to metabolic syndrome (MetS).
Models were established by providing Sprague–Dawley rats with high fat diet (HFD) combined with metformin or not. All objects were killed 40 days later with prostatic tissue being removed, weighed before stained, as well as the expression level of insulin-like growth factor I (IGF-1) and receptor (IGF-1R) being measured, and the level of insulin resistance (IR) has also been evaluated.
Model has been successfully established. Level of prostatic hyperplasia and IR as well as IGF-1 and IGF-1R expressions in the blank and saline control subunits of HFD group was higher than that of normal diet group (P < 0.05). In the subunit of metformin, along with the suppression of IR, the level of prostatic hyperplasia and the expression of IGF-1 pathway have both decreased (P < 0.05).
MetS can promote the growth of prostate during the formation of central obesity and IR. IGF-1 pathway may have an important role in the induction of BPH following IR. The application of metformin can suppress the expression of IGF-1 and IGF-1R, thus preventing the promotive effect of IR on prostate tissue in animal model of MetS.
KeywordsBenign prostatic hyperplasia Metabolic syndrome Insulin-like growth factor I Receptor, IGF type 1 Insulin resistance Metformin
Relevant personnel from the department of pathology, laboratory animal center, and urology of Anhui provincial hospital have provided a great deal of help.
This study was funded by Natural Science Foundation of Anhui Province (1408085QH152).
Compliance with ethical standards
Conflict of interest
All the authors declare that they have no conflict of interest.
The use of animal in this research was approved by the ethics committee of experimental animal of Anhui medical university.
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