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Body size and serum levels of insulin and leptin in relation to the risk of benign prostatic hyperplasia.
J Urol 2002; 168(2):599-604JU

Abstract

PURPOSE

Obesity has been implicated in the etiology of benign and malignant prostatic growth due to its influence on metabolic and endocrine changes. Because obesity is an important determinant of serum levels of insulin and leptin (the product of the obesity gene Ob), we investigated the role of obesity and serum levels of insulin and leptin in benign prostatic hyperplasia (BPH) etiology.

MATERIALS AND METHODS

Fasting serum levels of insulin and leptin as well as the body mass index, a measure of overall obesity, and waist-to-hip ratio, an indicator of abdominal obesity, were determined in 200 men newly diagnosed with BPH who were hospitalized for surgery and in 302 randomly selected healthy male subjects from the population in Shanghai, China.

RESULTS

A higher waist-to-hip ratio and higher serum insulin were significantly associated with an increased risk of BPH. Relative to men in the lowest waist-to-hip ratio quartile (less than 0.856) those in the highest quartile (greater than 0.923) were at 2.4-fold risk (odds ratio 2.42, 95% confidence interval [CI] 1.34 to 4.37, test for trend p = 0.01). Similarly relative to men in the lowest quartile of insulin (less than 5.87 microU. per ml.) those in the highest quartile (greater than 9.76 microU. per ml.) were at significantly increased risk (odds ratio 2.47, 95% CI 1.35 to 4.54, test for trend p = 0.009). The effect of insulin on BPH risk was more pronounced in men in low and middle tertiles of the waist-to-hip ratio (odds ratios comparing high to low insulin tertiles 2.8 and 2.7, respectively), while among men in the highest waist-to-hip ratio tertile insulin was not significantly associated with BPH risk. In contrast, we found no significant odds ratio comparing the highest to lowest quartiles of leptin (odds ratio 0.62, 95% CI 0.33 to 1.17) or body mass index (odds ratio 1.64, 95% CI 0.96 to 2.81).

CONCLUSIONS

Our results suggest that abdominal obesity and increasing serum insulin, and possibly overall obesity but not serum leptin are associated with a higher risk of BPH. Further prospective and laboratory studies are needed to confirm these results and elucidate the underlying mechanisms.

Authors+Show Affiliations

Department of Epidemiology and Biostatistics, School of Public Health and Health Sciences, George Washington University, Washington, DC, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

12131317

Citation

Dahle, Sara E., et al. "Body Size and Serum Levels of Insulin and Leptin in Relation to the Risk of Benign Prostatic Hyperplasia." The Journal of Urology, vol. 168, no. 2, 2002, pp. 599-604.
Dahle SE, Chokkalingam AP, Gao YT, et al. Body size and serum levels of insulin and leptin in relation to the risk of benign prostatic hyperplasia. J Urol. 2002;168(2):599-604.
Dahle, S. E., Chokkalingam, A. P., Gao, Y. T., Deng, J., Stanczyk, F. Z., & Hsing, A. W. (2002). Body size and serum levels of insulin and leptin in relation to the risk of benign prostatic hyperplasia. The Journal of Urology, 168(2), pp. 599-604.
Dahle SE, et al. Body Size and Serum Levels of Insulin and Leptin in Relation to the Risk of Benign Prostatic Hyperplasia. J Urol. 2002;168(2):599-604. PubMed PMID: 12131317.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Body size and serum levels of insulin and leptin in relation to the risk of benign prostatic hyperplasia. AU - Dahle,Sara E, AU - Chokkalingam,Anand P, AU - Gao,Yu-Tang, AU - Deng,Jie, AU - Stanczyk,Frank Z, AU - Hsing,Ann W, PY - 2002/7/20/pubmed PY - 2002/8/17/medline PY - 2002/7/20/entrez SP - 599 EP - 604 JF - The Journal of urology JO - J. Urol. VL - 168 IS - 2 N2 - PURPOSE: Obesity has been implicated in the etiology of benign and malignant prostatic growth due to its influence on metabolic and endocrine changes. Because obesity is an important determinant of serum levels of insulin and leptin (the product of the obesity gene Ob), we investigated the role of obesity and serum levels of insulin and leptin in benign prostatic hyperplasia (BPH) etiology. MATERIALS AND METHODS: Fasting serum levels of insulin and leptin as well as the body mass index, a measure of overall obesity, and waist-to-hip ratio, an indicator of abdominal obesity, were determined in 200 men newly diagnosed with BPH who were hospitalized for surgery and in 302 randomly selected healthy male subjects from the population in Shanghai, China. RESULTS: A higher waist-to-hip ratio and higher serum insulin were significantly associated with an increased risk of BPH. Relative to men in the lowest waist-to-hip ratio quartile (less than 0.856) those in the highest quartile (greater than 0.923) were at 2.4-fold risk (odds ratio 2.42, 95% confidence interval [CI] 1.34 to 4.37, test for trend p = 0.01). Similarly relative to men in the lowest quartile of insulin (less than 5.87 microU. per ml.) those in the highest quartile (greater than 9.76 microU. per ml.) were at significantly increased risk (odds ratio 2.47, 95% CI 1.35 to 4.54, test for trend p = 0.009). The effect of insulin on BPH risk was more pronounced in men in low and middle tertiles of the waist-to-hip ratio (odds ratios comparing high to low insulin tertiles 2.8 and 2.7, respectively), while among men in the highest waist-to-hip ratio tertile insulin was not significantly associated with BPH risk. In contrast, we found no significant odds ratio comparing the highest to lowest quartiles of leptin (odds ratio 0.62, 95% CI 0.33 to 1.17) or body mass index (odds ratio 1.64, 95% CI 0.96 to 2.81). CONCLUSIONS: Our results suggest that abdominal obesity and increasing serum insulin, and possibly overall obesity but not serum leptin are associated with a higher risk of BPH. Further prospective and laboratory studies are needed to confirm these results and elucidate the underlying mechanisms. SN - 0022-5347 UR - https://www.unboundmedicine.com/medline/citation/12131317/full_citation L2 - https://linkinghub.elsevier.com/retrieve/pii/S0022-5347(05)64687-3 DB - PRIME DP - Unbound Medicine ER -