Up-regulation of hepatic IGFBP-1 production as a strategy for preventing benign prostatic hyperplasia

Abstract 

Many lines of evidence point to a prominent role for excess production and activity of stroma-derived, androgen-induced IGF-II in the stromal and epithelial hyperplasia characteristic of benign prostatic hyperplasia (BPH). Increased stromal expression of the type I IGF receptor, as well as altered local production of IGF binding proteins, appear to contribute to this increase in IGF activity. Systemic IGFBP-1, primarily of hepatic origin, is a functional antagonist of IGF-II; thus, boosting IGFBP-1 production might be expected to lessen risk for BPH. Minimizing diurnal insulin secretion, and possibly avoiding intake of animal proteins over-rich in essential amino acids, are practical strategies for increasing hepatic IGFBP-1 synthesis. This hypothesis may rationalize recent evidence that exercise and moderate alcohol consumption decrease risk for BPH, whereas heavy smoking increases this risk. A clinical impression that BPH is becoming more common in Japan, and evidence that Japanese making frequent use of meat and dairy products are at increased risk for this disorder, also appear consistent with this view.

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