Interactions between diet and peroxisome proliferator-activated receptor-gamma gene Pro12Ala and C161T polymorphisms on prostate cancer risk in Japanese men

背景。前列腺癌可能是由高脂肪消耗和影响脂质代谢的基因多态性（如过氧化物酶体增殖物激活受体γ (PPAR-γ)基因）之间的相互作用引起的。我们研究了饮食、PPAR-γ基因多态性（Pro12Ala和C161T）以及基因-饮食相互作用与日本人前列腺癌风险的关系。方法。样本来自新诊断的110例前列腺癌患者和214例活检阴性对照。比较了病例组和对照组的日能量和常量营养素消耗量。我们使用逻辑回归分析，根据每个多态性的基因型估计前列腺癌风险的优势比（OR）和95%置信区间（CI）。证实了低/高营养摄入与PPAR-γ基因多态性在前列腺癌风险中的相互作用。结果。实验组和对照组的日能量和常量营养素摄取量无显著差异。Pro12Ala多态性与前列腺癌风险无关。相反，C161T替代与前列腺癌风险降低相关。携带C161T的T等位基因对前列腺癌有保护作用（多重校正OR: 0.53, 95% CI: 0.31-0.93）。在低脂或碳水化合物摄入组中，C161T等位基因携带者降低了前列腺癌的风险（多重校正or （95% CI）分别为0.33（0.13-0.83）和0.42(0.18-0.97)）。然而，营养摄入与前列腺癌风险的PPAR-γ基因多态性之间没有相互作用。PPAR-γ基因C161T替代与日本人前列腺癌风险降低相关然而，Pro12Ala多态性未见显著关联。低脂肪或碳水化合物的摄入可能会加强C161T替代的风险降低。

Background. Prostate cancer could be arisen from interactions between high fat consumption and gene polymorphisms influencing lipid metabolism, such as peroxisome proliferator-activated receptor gamma (PPAR-γ) gene. We examined associations of diet, PPAR-γ gene polymorphisms (Pro12Ala and C161T) and the gene-diet interactions on prostate cancer risk in Japanese. Methods. Samples were obtained from newly diagnosed 110 prostate cancer cases and 214 biopsy-negative controls. Daily consumption of energy and macronutrients were compared between cases and controls. We used logistic regression analysis to estimate the odds ratio (OR) and 95% confidence interval (CI) for prostate cancer risk according to genotype of each polymorphism. Interactions between low/high nutrient intakes and PPAR-γ gene polymorphisms on prostate cancer risk were proved. Results. Daily intake of energy and macronutrients were not different between cases and controls. Pro12Ala polymorphism was not associated with prostate cancer risk. In contrast, C161T substitution was associated with reduced prostate cancer risk. The T allele carriers of C161T showed a protective effect (multiple-adjusted OR: 0.53, 95% CI: 0.31-0.93) on prostate cancer. Among low fat or carbohydrate intake groups, the T allele carriers of C161T reduced prostate cancer risk (multiple-adjusted OR (95% CI): 0.33 (0.13-0.83) and 0.42 (0.18-0.97), respectively). However, there were no interactions between consumption of nutrients and PPAR-γ gene polymorphisms for prostate cancer risk.Conclusions. PPAR-γ gene C161T substitution was associated with decreased prostate cancer risk in Japanese; however, no significant link was observed for Pro12Ala polymorphism. Low intake of fat or carbohydrate may strength the risk reduction by C161T substitution.