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Prostate cancer: another aspect of the insulin-resistance syndrome?

Authors


Address reprint requests to: RJ Barnard, Department of Physiological Science, UCLA, 621 Charles E. Young Dr So, Los Angeles, CA 90095-1606, USA. E-mail: jbarnard@physci.ucla.edu

Summary

Insulin resistance and compensatory hyperinsulinaemia are thoughtto be the underlying factors in the metabolic or insulin-resistancesyndrome and can be controlled by diet and exercise. Hyperinsulinaemiahas been shown to have a direct effect on the liver, suppressingthe production of sex hormone-binding globulin (SHBG) and insulin-likegrowth factor-binding proteins 1 and 2 (IGFBP-1, -2) while stimulatingthe production of insulin-like growth factor 1 (IGF-1). These factorshave been proposed to be important modulators of hormone-related cancers,such as prostate cancer. Men adopting a low-fat diet and daily exercise reducedtheir levels of serum insulin and IGF-1, while increasing theirlevels of IGFBP-1 and sex hormone-binding globulin (SHBG). Cell-culturestudies with LNCaP prostate cancer cells showed apoptosis of tumourcells and a reduction in serum-stimulated cell growth in the postdiet and exercise serum. These results suggest that prostate cancermay be another aspect of the insulin-resistance syndrome and thatadopting a low-fat diet combined with regular exercise may reducethe risk for prostate and other hormone-related cancers. This needsto be tested with prospective studies.

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