Department of Social and Preventive Medicine, Julius Centre University of Malaya, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia; Department of Epidemiology and Welch Center for Prevention, Epidemiology, and Clinical Research, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland.
Center for Health Promotion, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, South Korea.
Gastroenterology. 2014 Jul;147(1):78-87.e3. doi: 10.1053/j.gastro.2014.03.006. Epub 2014 Mar 14.
BACKGROUND & AIMS: Diabetes is a risk factor for colorectal cancer. We studied the association between markers of glucose metabolism and metabolic syndrome and the presence of colorectal adenomas in a large number of asymptomatic men and women attending a health screening program in South Korea. We also investigated whether these associations depend on adenoma location.
In a cross-sectional study, we measured fasting levels of glucose, insulin, hemoglobin A1c, and C-peptide and calculated homeostatic model assessment (HOMA) values (used to quantify insulin resistance) for 19,361 asymptomatic South Korean subjects who underwent colonoscopy examinations from January 2006 to June 2009. Participants completed a standardized self-administered health questionnaire and a validated semiquantitative food frequency questionnaire. Blood samples were collected on the day of the colonoscopy; fasting blood samples were also collected. Robust Poisson regression was used to model the associations of glucose markers with the prevalence of any adenoma.
Using detailed multivariable-adjusted dose-response models, the prevalence ratios (aPR, 95% confidence interval [CI]) for any adenoma, comparing the 90th with the 10th percentile, were 1.08 (1.00-1.16; P = .04) for fasting glucose, 1.07 (0.99-1.15; P = .10) for insulin, 1.09 (1.02-1.18, P = .02) for HOMA, 1.09 (1.01-1.17; P = .02) for hemoglobin A1c, and 1.14 (1.05-1.24; P = .002) for C-peptide. The corresponding ratios for nonadvanced adenomas were 1.11 (0.99-1.25; P = .08), 1.10 (0.98-1.24; P = .12), 1.15 (1.02-1.29; P = .02), 1.14 (1.01-1.28; P = .03), and 1.20 (1.05-1.37; P = .007), respectively. The corresponding ratios for advanced adenomas were 1.32 (0.94-1.84; P = .11), 1.23 (0.87-1.75; P = .24), 1.30 (0.92-1.85; P = .14), 1.13 (0.79-1.61; P = .50), and 1.67 (1.15-2.42; P = .007), respectively. Metabolic syndrome was associated with the prevalence of any adenoma (aPR, 1.18; 95% CI, 1.13-1.24; P < .001), nonadvanced adenoma (aPR, 1.30; 95% CI, 1.20-1.40; P < .001), and advanced adenoma (aPR, 1.42; 95% CI, 1.14-1.78; P = .002). Associations were similar for adenomas located in the distal versus proximal colon.
Increasing levels of glucose, HOMA values, levels of hemoglobin A1c and C-peptide, and metabolic syndrome are significantly associated with the prevalence of adenomas. Adenomas should be added to the list of consequences of altered glucose metabolism.
糖尿病是结直肠癌的一个危险因素。我们研究了大量在韩国参加健康筛查计划的无症状男性和女性中,葡萄糖代谢和代谢综合征标志物与结直肠腺瘤存在之间的关系。我们还研究了这些关联是否取决于腺瘤的位置。
在一项横断面研究中,我们测量了 19361 名无症状韩国受试者的空腹血糖、胰岛素、糖化血红蛋白和 C 肽水平,并计算了用于量化胰岛素抵抗的稳态模型评估(HOMA)值,这些受试者于 2006 年 1 月至 2009 年 6 月接受了结肠镜检查。参与者完成了标准化的自我管理健康问卷和经过验证的半定量食物频率问卷。在结肠镜检查当天采集血样;也采集了空腹血样。使用稳健泊松回归模型来模拟葡萄糖标志物与任何腺瘤患病率之间的关联。
使用详细的多变量调整剂量反应模型,与第 10 百分位相比,第 90 百分位的任何腺瘤患病率比(aPR,95%置信区间[CI])分别为空腹血糖 1.08(1.00-1.16;P =.04)、胰岛素 1.07(0.99-1.15;P =.10)、HOMA 1.09(1.02-1.18,P =.02)、糖化血红蛋白 1.09(1.01-1.17;P =.02)和 C 肽 1.14(1.05-1.24;P =.002)。非高级腺瘤的相应比值分别为 1.11(0.99-1.25;P =.08)、1.10(0.98-1.24;P =.12)、1.15(1.02-1.29;P =.02)、1.14(1.01-1.28;P =.03)和 1.20(1.05-1.37;P =.007)。高级腺瘤的相应比值分别为 1.32(0.94-1.84;P =.11)、1.23(0.87-1.75;P =.24)、1.30(0.92-1.85;P =.14)、1.13(0.79-1.61;P =.50)和 1.67(1.15-2.42;P =.007)。代谢综合征与任何腺瘤(aPR,1.18;95%CI,1.13-1.24;P <.001)、非高级腺瘤(aPR,1.30;95%CI,1.20-1.40;P <.001)和高级腺瘤(aPR,1.42;95%CI,1.14-1.78;P =.002)的患病率显著相关。远端结肠和近端结肠的腺瘤位置相似。
葡萄糖、HOMA 值、糖化血红蛋白和 C 肽水平以及代谢综合征水平的升高与腺瘤的患病率显著相关。腺瘤应被添加到改变的葡萄糖代谢的后果列表中。