Serum adiponectin, C-peptide and leptin and risk of symptomatic benign prostatic hyperplasia

Results from the prostate cancer prevention trial

Jeannette M. Schenk, Alan R. Kristal, Marian L. Neuhouser, Catherine M. Tangen, Emily White, Daniel W. Lin, Ian M. Thompson

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

BACKGROUND. Recent epidemiologic studies have identified obesity as a risk factor for benign prostatic hyperplasia (BPH). We examined whether adiponectin, leptin, and C-peptide were associated with incident, symptomatic BPH and whether these factors mediate the relationship between obesity and BPH risk. METHODS. Data are from Prostate Cancer Prevention Trial placebo arm participants who were free of BPH at baseline. Incident BPH(n = 698) was defined as treatment, two International Prostate Symptom Score (IPSS) values>14, or an increase of ≥5 in IPSS from baseline documented on at least two occasions plus at least one score ≥12. Controls (n = 709) were selected from men reporting no BPH treatment or IPSS> 7 during the 7-year trial. Baseline serum was analyzed for adiponectin, C-peptide, and leptin concentrations. RESULTS. Neither C-peptide nor leptin was associated with BPH risk. The odds ratio [95% CI] contrasting highest to lowest quartiles of adiponectin was 0.65[0.47, 0.87] P trend=0.004. Findings differed between levels of physical activity: there was a strong inverse association between adiponectin and BPH among moderately/very active men OR = 0.43 [0.29, 0.63], and no association among sedentary/minimally active men OR = 0.92 [0.65, 1.30] Pinteraction = 0.005. Adiponectin concentrations explained only a moderate amount of the relationship between obesity and BPH risk. CONCLUSIONS. High adiponectin concentrations were associated with reduced risk of incident, symptomatic BPH. This association was limited to moderately/very active men; suggesting the relationship between obesity and BPH involves a complex interaction between factors affecting glucose uptake and insulin sensitivity. However, adiponectin is likely not the only mechanism through which obesity affects BPH risk.

Original languageEnglish (US)
Pages (from-to)1303-1311
Number of pages9
JournalProstate
Volume69
Issue number12
DOIs
StatePublished - Sep 1 2009

Fingerprint

C-Peptide
Adiponectin
Prostatic Hyperplasia
Leptin
Prostatic Neoplasms
Serum
Obesity
Prostate
Insulin Resistance
Epidemiologic Studies
Odds Ratio
Placebos
Exercise

Keywords

  • Benign prostatic hyperplasia
  • Insulin resistance
  • Lower urinary tract symptoms
  • Obesity

ASJC Scopus subject areas

  • Urology
  • Oncology

Cite this

Schenk, J. M., Kristal, A. R., Neuhouser, M. L., Tangen, C. M., White, E., Lin, D. W., & Thompson, I. M. (2009). Serum adiponectin, C-peptide and leptin and risk of symptomatic benign prostatic hyperplasia: Results from the prostate cancer prevention trial. Prostate, 69(12), 1303-1311. https://doi.org/10.1002/pros.20974

Serum adiponectin, C-peptide and leptin and risk of symptomatic benign prostatic hyperplasia : Results from the prostate cancer prevention trial. / Schenk, Jeannette M.; Kristal, Alan R.; Neuhouser, Marian L.; Tangen, Catherine M.; White, Emily; Lin, Daniel W.; Thompson, Ian M.

In: Prostate, Vol. 69, No. 12, 01.09.2009, p. 1303-1311.

Research output: Contribution to journalArticle

Schenk, JM, Kristal, AR, Neuhouser, ML, Tangen, CM, White, E, Lin, DW & Thompson, IM 2009, 'Serum adiponectin, C-peptide and leptin and risk of symptomatic benign prostatic hyperplasia: Results from the prostate cancer prevention trial', Prostate, vol. 69, no. 12, pp. 1303-1311. https://doi.org/10.1002/pros.20974
Schenk, Jeannette M. ; Kristal, Alan R. ; Neuhouser, Marian L. ; Tangen, Catherine M. ; White, Emily ; Lin, Daniel W. ; Thompson, Ian M. / Serum adiponectin, C-peptide and leptin and risk of symptomatic benign prostatic hyperplasia : Results from the prostate cancer prevention trial. In: Prostate. 2009 ; Vol. 69, No. 12. pp. 1303-1311.
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abstract = "BACKGROUND. Recent epidemiologic studies have identified obesity as a risk factor for benign prostatic hyperplasia (BPH). We examined whether adiponectin, leptin, and C-peptide were associated with incident, symptomatic BPH and whether these factors mediate the relationship between obesity and BPH risk. METHODS. Data are from Prostate Cancer Prevention Trial placebo arm participants who were free of BPH at baseline. Incident BPH(n = 698) was defined as treatment, two International Prostate Symptom Score (IPSS) values>14, or an increase of ≥5 in IPSS from baseline documented on at least two occasions plus at least one score ≥12. Controls (n = 709) were selected from men reporting no BPH treatment or IPSS> 7 during the 7-year trial. Baseline serum was analyzed for adiponectin, C-peptide, and leptin concentrations. RESULTS. Neither C-peptide nor leptin was associated with BPH risk. The odds ratio [95{\%} CI] contrasting highest to lowest quartiles of adiponectin was 0.65[0.47, 0.87] P trend=0.004. Findings differed between levels of physical activity: there was a strong inverse association between adiponectin and BPH among moderately/very active men OR = 0.43 [0.29, 0.63], and no association among sedentary/minimally active men OR = 0.92 [0.65, 1.30] Pinteraction = 0.005. Adiponectin concentrations explained only a moderate amount of the relationship between obesity and BPH risk. CONCLUSIONS. High adiponectin concentrations were associated with reduced risk of incident, symptomatic BPH. This association was limited to moderately/very active men; suggesting the relationship between obesity and BPH involves a complex interaction between factors affecting glucose uptake and insulin sensitivity. However, adiponectin is likely not the only mechanism through which obesity affects BPH risk.",
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N2 - BACKGROUND. Recent epidemiologic studies have identified obesity as a risk factor for benign prostatic hyperplasia (BPH). We examined whether adiponectin, leptin, and C-peptide were associated with incident, symptomatic BPH and whether these factors mediate the relationship between obesity and BPH risk. METHODS. Data are from Prostate Cancer Prevention Trial placebo arm participants who were free of BPH at baseline. Incident BPH(n = 698) was defined as treatment, two International Prostate Symptom Score (IPSS) values>14, or an increase of ≥5 in IPSS from baseline documented on at least two occasions plus at least one score ≥12. Controls (n = 709) were selected from men reporting no BPH treatment or IPSS> 7 during the 7-year trial. Baseline serum was analyzed for adiponectin, C-peptide, and leptin concentrations. RESULTS. Neither C-peptide nor leptin was associated with BPH risk. The odds ratio [95% CI] contrasting highest to lowest quartiles of adiponectin was 0.65[0.47, 0.87] P trend=0.004. Findings differed between levels of physical activity: there was a strong inverse association between adiponectin and BPH among moderately/very active men OR = 0.43 [0.29, 0.63], and no association among sedentary/minimally active men OR = 0.92 [0.65, 1.30] Pinteraction = 0.005. Adiponectin concentrations explained only a moderate amount of the relationship between obesity and BPH risk. CONCLUSIONS. High adiponectin concentrations were associated with reduced risk of incident, symptomatic BPH. This association was limited to moderately/very active men; suggesting the relationship between obesity and BPH involves a complex interaction between factors affecting glucose uptake and insulin sensitivity. However, adiponectin is likely not the only mechanism through which obesity affects BPH risk.

AB - BACKGROUND. Recent epidemiologic studies have identified obesity as a risk factor for benign prostatic hyperplasia (BPH). We examined whether adiponectin, leptin, and C-peptide were associated with incident, symptomatic BPH and whether these factors mediate the relationship between obesity and BPH risk. METHODS. Data are from Prostate Cancer Prevention Trial placebo arm participants who were free of BPH at baseline. Incident BPH(n = 698) was defined as treatment, two International Prostate Symptom Score (IPSS) values>14, or an increase of ≥5 in IPSS from baseline documented on at least two occasions plus at least one score ≥12. Controls (n = 709) were selected from men reporting no BPH treatment or IPSS> 7 during the 7-year trial. Baseline serum was analyzed for adiponectin, C-peptide, and leptin concentrations. RESULTS. Neither C-peptide nor leptin was associated with BPH risk. The odds ratio [95% CI] contrasting highest to lowest quartiles of adiponectin was 0.65[0.47, 0.87] P trend=0.004. Findings differed between levels of physical activity: there was a strong inverse association between adiponectin and BPH among moderately/very active men OR = 0.43 [0.29, 0.63], and no association among sedentary/minimally active men OR = 0.92 [0.65, 1.30] Pinteraction = 0.005. Adiponectin concentrations explained only a moderate amount of the relationship between obesity and BPH risk. CONCLUSIONS. High adiponectin concentrations were associated with reduced risk of incident, symptomatic BPH. This association was limited to moderately/very active men; suggesting the relationship between obesity and BPH involves a complex interaction between factors affecting glucose uptake and insulin sensitivity. However, adiponectin is likely not the only mechanism through which obesity affects BPH risk.

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