School of Public Health, Xinjiang Medical University, Urumqi, China.
Department of Urology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Front Endocrinol (Lausanne). 2024 Aug 6;15:1442740. doi: 10.3389/fendo.2024.1442740. eCollection 2024.
Obesity-induced metabolic dysfunction increases the risk of developing tumors, however, the relationship between metabolic obesity phenotypes and prostate cancer (PCa) remains unclear.
The term metabolic obesity phenotypes was introduced based on metabolic status and BMI categories. Participants were categorized into four groups: metabolically healthy nonobesity (MHNO), metabolically healthy obesity (MHO), metabolically unhealthy nonobesity (MUNO), and metabolically unhealthy obesity (MUO). Propensity score matching was conducted based on age, ethnicity, marriage, etc. Univariate and multivariate conditional logistic regression analyses were used to assess the relationship between metabolic obesity phenotypes, metabolic risk factors, and PCa. Sensitivity analysis was performed to verify the robustness of the results.
After propensity score matching among 564 PCa patients and 1418 healthy individuals, 209 were selected for each of the case and control groups. There were no statistically significant differences in the basic characteristics between the two groups. Univariate and multivariate conditional logistic regression suggested that the risk of developing PCa in both MHO and MUO individuals was higher than in MHNO individuals. Specifically, the risk of developing PCa in MHO individuals was 2.166 times higher than in MHNO individuals (OR=2.166, 95%CI: 1.133-4.139), and the risk in MUO individuals was is 2.398 times higher than in MHNO individuals(OR=2.398, 95%CI:1.271-4.523). Individuals with hyperglycemia and elevated triglycerides also had a higher risk of developing PCa (hyperglycemia:OR=1.488, 95%CI: 1.001-2.210; elevated triglycerides: OR=2.292, 95%CI: 1.419-3.702). Those with more than or equal to three metabolic risk factors had an increased risk of PCa (OR=1.990, 95%CI: 1.166-3.396). Sensitivity analysis indicated an increased risk of PCa in MUO individuals compared to MHNO individuals.
In this retrospective study, individuals with MHO and MUO had a higher risk of developing PCa.
肥胖引起的代谢功能障碍增加了肿瘤发生的风险，然而，代谢性肥胖表型与前列腺癌（PCa）之间的关系尚不清楚。
基于代谢状态和 BMI 类别引入代谢性肥胖表型这一术语。参与者被分为四组：代谢健康非肥胖（MHNO）、代谢健康肥胖（MHO）、代谢不健康非肥胖（MUNO）和代谢不健康肥胖（MUO）。根据年龄、种族、婚姻等进行倾向评分匹配。使用单变量和多变量条件逻辑回归分析来评估代谢性肥胖表型、代谢风险因素与 PCa 之间的关系。进行敏感性分析以验证结果的稳健性。
在对 564 例 PCa 患者和 1418 例健康个体进行倾向评分匹配后，选择了 209 例病例组和 209 例对照组。两组的基本特征无统计学差异。单变量和多变量条件逻辑回归表明，MHO 和 MUO 个体患 PCa 的风险均高于 MHNO 个体。具体而言，MHO 个体患 PCa 的风险是 MHNO 个体的 2.166 倍（OR=2.166，95%CI：1.133-4.139），MUO 个体的风险是 MHNO 个体的 2.398 倍（OR=2.398，95%CI：1.271-4.523）。患有高血糖和甘油三酯升高的个体患 PCa 的风险也更高（高血糖：OR=1.488，95%CI：1.001-2.210；甘油三酯升高：OR=2.292，95%CI：1.419-3.702）。有超过或等于三种代谢风险因素的个体患 PCa 的风险增加（OR=1.990，95%CI：1.166-3.396）。敏感性分析表明，MUO 个体患 PCa 的风险高于 MHNO 个体。
在这项回顾性研究中，MHO 和 MUO 个体患 PCa 的风险较高。
