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Int Urol Nephrol. 2018 Apr;50(4):611-617. doi: 10.1007/s11255-018-1826-9. Epub 2018 Feb 19.

Effects of metformin on prostatic tissue of rats with metabolic syndrome and benign prostatic hyperplasia.

Author information

1
Department of Urology, Anhui Provincial Hospital, The First Affiliated Hospital of University of Science and Technology of China, #17 Lujiang Road, Hefei, 230001, China.
2
Department of Pathology, Anhui Provincial Hospital, The First Affiliated Hospital of University of Science and Technology of China, #17 Lujiang Road, Hefei, 230001, China.
3
Department of Urology, Anhui Provincial Hospital, The First Affiliated Hospital of University of Science and Technology of China, #17 Lujiang Road, Hefei, 230001, China. dramantony@126.com.

Abstract

OBJECTIVES:

To investigate the efficacy of insulin sensitizer on prostatic tissue in animal model with benign prostatic hyperplasia (BPH) secondary to metabolic syndrome (MetS).

METHODS:

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.

RESULTS:

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).

CONCLUSION:

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.

KEYWORDS:

Benign prostatic hyperplasia; Insulin resistance; Insulin-like growth factor I; Metabolic syndrome; Metformin; Receptor, IGF type 1

PMID:
29460133
DOI:
10.1007/s11255-018-1826-9
[Indexed for MEDLINE]

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