Schenk Jeannette M, Kristal Alan R, Neuhouser Marian L, Tangen Catherine M, White Emily, Lin Daniel W, Thompson Ian M
Fred Hutchinson Cancer Research Center, Cancer Prevention Program, Seattle, Washington 98109-1024, USA.
Prostate. 2009 Sep 1;69(12):1303-11. doi: 10.1002/pros.20974.
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.
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 >or=5 in IPSS from baseline documented on at least two occasions plus at least one score >or=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.
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] P(interaction) = 0.005. Adiponectin concentrations explained only a moderate amount of the relationship between obesity and BPH risk.
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.
近期的流行病学研究已将肥胖确定为良性前列腺增生（BPH）的一个风险因素。我们研究了脂联素、瘦素和C肽是否与新发有症状BPH相关，以及这些因素是否介导肥胖与BPH风险之间的关系。
数据来自前列腺癌预防试验安慰剂组的参与者，他们在基线时无BPH。新发BPH（n = 698）定义为接受治疗、两次国际前列腺症状评分（IPSS）值>14，或IPSS较基线至少增加≥5（至少两次记录）且至少有一次评分≥12。对照组（n = 709）从在7年试验期间报告未接受BPH治疗或IPSS>7的男性中选取。分析基线血清中的脂联素、C肽和瘦素浓度。
C肽和瘦素均与BPH风险无关。脂联素最高四分位数与最低四分位数相比的比值比[95%可信区间]为0.65[0.47, 0.87]，P（趋势）= 0.004。体力活动水平不同，结果也不同：在中度/非常活跃的男性中，脂联素与BPH之间存在强烈的负相关，OR = 0.43[0.29, 0.63]，而在久坐/极少活动的男性中无相关性，OR = 0.92[0.65, 1.30]，P（交互作用）= 0.005。脂联素浓度仅解释了肥胖与BPH风险之间关系的一部分。
高浓度脂联素与新发有症状BPH风险降低相关。这种关联仅限于中度/非常活跃的男性；提示肥胖与BPH之间的关系涉及影响葡萄糖摄取和胰岛素敏感性的因素之间的复杂相互作用。然而，脂联素可能不是肥胖影响BPH风险的唯一机制。
