Diabetes, growth hormone-insulin-like growth factor pathways and association to
benign prostatic hyperplasia.
Authors Wang Z, Olumi AF
Submitted By Aria Olumi on 2/22/2012
Status Published
Journal Differentiation; research in biological diversity
Year 2011
Date Published 8/1/2011
Volume : Pages 82 : 261 - 271
PubMed Reference 21536370
Abstract Diabetes significantly increases the risk of benign prostatic hyperplasia (BPH)
and low urinary tract symptoms (LUTS). The major endocrine aberration in
connection with the metabolic syndrome is hyperinsulinemia. Insulin is an
independent risk factor and a promoter of BPH. Insulin resistance may change the
risk of BPH through several biological pathways. Hyperinsulinemia stimulates the
liver to produce more insulin-like growth factor (IGF), another mitogen and an
anti-apoptotic agent which binds insulin receptor/IGF receptor and stimulates
prostate growth. The levels of IGFs and IGF binding proteins (IGFBPs) in
prostate tissue and in blood are associated with BPH risk, with the regulation
of circulating androgen and growth hormone. Stromal-epithelial interactions play
a critical role in the development and growth of the prostate gland and BPH.
Previously, we have shown that the expression of c-Jun in the fibroblastic
stroma can promote secretion of IGF-I, which stimulates prostate epithelial cell
proliferation through activating specific target genes. Here, we will review the
epidemiologic, clinical, and molecular findings which have evaluated the
relation between diabetes and development of BPH.

Investigators with authorship
Aria OlumiBeth Israel Deaconess Medical