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Letter to the editor |
Division of Endocrinology and Metabolism, Harbor-University of California Los Angeles Medical Center and Los Angeles Biomedical Research Institute, David Geffen School of Medicine at University of California Los Angeles, Torrance, California 90509-2910
Address correspondence to: Dr. Christina C. Wang, Harbor-University of California Los Angeles Medical Center, Clinical Study Center (Box 16), 1000 West Carson Street, Torrance, California 90509-2910. E-mail: wang{at}labiomed.org.
To the editors:
We thank Dr. Seshadri (1) for his thoughtful comments on the possible role of leptin in a high-fat diet and the risk of prostate cancer. We do not fully understand how dietary fat modulation impacts androgen secretion and prostate cancer risk. Our study was not designed to address this question. In the manuscript, our suggestions of the possible mechanisms of action of diet modulation from high to low fat on androgens include: the lowering of the substrates or their metabolism resulting in lower androgen production, the minimal suppression of the gonadotropins, and the possible direct effects of changes in fatty acid composition on androgen production (2). We agree that studies to examine the pulsatile secretion of the gonadotropins were not the goals of the study, and subtle changes in the pulsatile secretion of LH may impact testicular testosterone production. We argue that this may be unlikely, given the very small decreases in mean serum gonadotropins that may not be of any clinical consequence.
Dr. Seshadri introduced the possible role of leptin in the changes in androgen concentrations after a low-fat diet. In short-term starvation studies, leptin levels fall (3), whereas a high-fat diet reduces leptin levels (4). The suggestion that a low-fat diet induces higher serum leptin levels that in turn may contribute to the lower androgen levels is interesting. Our laboratory is considering measuring leptin and other adipose tissues, factors that might be involved in androgen metabolism. The association between high leptin levels in vivo and in vitro and prostate cancer risk (5, 6) is interesting, but a causal relationship has not been demonstrated. We agree that more clinical research on the mechanisms by which dietary fat modulation influences intraprostatic androgen metabolism is required; leptin and others could be considered as candidate intermediaries.
Received April 7, 2005.
References
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C. Wang and R. S. Swerdloff Authors' Response: Dietary Fat and Androgens J. Clin. Endocrinol. Metab., June 1, 2005; 90(6): 3802 - 3802. [Full Text] [PDF] |
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