Department of Nutrition and Dietetics, School of Health Science and Education, Harokopio University, Athens, Greece.
First Cardiology Clinic, School of Medicine, University of Athens, Athens, Greece.
Diabetes Metab Res Rev. 2018 Jan;34(1). doi: 10.1002/dmrr.2939. Epub 2017 Sep 25.
The role of inflammation in diabetes development is not fully elucidated. The aim of this work was to investigate the independent effect of individual inflammatory markers and combinations of them on diabetes incidence and the potential mediating role of obesity.
In 2001 to 2002, a random sample of 1514 men (18-87 years old) and 1528 women (18-89 years old) was selected to participate in the ATTICA study, where Athens is a major metropolis. Interleukin-6 (IL-6), C-reactive protein (CRP), tumour necrosis factor-alpha, serum amyloid alpha, fibrinogen, and homocysteine were measured. Covariates included various clinical, demographic, and lifestyle characteristics, assessed with standard procedures. In 2012, the 10 year follow-up was performed. Diabetes diagnosis was defined according to American Diabetes Association criteria among n = 1485 participants.
One hundred ninety-one incident cases of diabetes were documented, yielding an incidence of 12.9% (13.4% in men and 12.4% in women). After adjustments, only elevated IL-6 increased by 2.2 times the 10 year diabetes risk (third vs first tertile, 95% CI: 1.13, 4.28). After investigating combinations of inflammatory markers, combined elevated levels of CRP and IL-6 or CRP and fibrinogen (both markers ≥75th percentile vs <75th percentile) increased the risk by 1.93 times (95% CI: 1.20, 3.08) and 2.37 times (95% CI: 1.37, 4.16), respectively. Body mass index was found to significantly mediate the aggravating effect of inflammation.
The reported results underline the significant role of individual IL-6 or combinations of CRP-IL-6 and CRP-fibrinogen in diabetes prediction. Adiposity seems to be primarily responsible for an increase in inflammatory markers, leading through this mechanism to insulin resistance and increasing diabetes risk.
炎症在糖尿病发展中的作用尚未完全阐明。本研究旨在探讨单个炎症标志物及其组合对糖尿病发病的独立影响，以及肥胖的潜在中介作用。
2001 年至 2002 年，随机抽取 1514 名男性（18-87 岁）和 1528 名女性（18-89 岁）参加 ATTICA 研究，该研究地点在雅典大都市。测量白细胞介素-6（IL-6）、C 反应蛋白（CRP）、肿瘤坏死因子-α、血清淀粉样蛋白 α、纤维蛋白原和同型半胱氨酸。协变量包括各种临床、人口统计学和生活方式特征，通过标准程序进行评估。2012 年进行了 10 年随访。根据美国糖尿病协会标准，在 n=1485 名参与者中诊断为糖尿病。
记录了 191 例糖尿病发病病例，发病率为 12.9%（男性为 13.4%，女性为 12.4%）。调整后，仅升高的 IL-6 使 10 年糖尿病风险增加 2.2 倍（第三与第一三分位数，95%CI：1.13，4.28）。在研究炎症标志物组合后，CRP 和 IL-6 或 CRP 和纤维蛋白原（两个标志物均≥75 百分位）水平升高组合使风险增加 1.93 倍（95%CI：1.20，3.08）和 2.37 倍（95%CI：1.37，4.16）。体重指数被发现可显著介导炎症的加重作用。
报告结果强调了个体 IL-6 或 CRP-IL-6 和 CRP-纤维蛋白原组合在糖尿病预测中的重要作用。肥胖似乎是导致炎症标志物升高的主要原因，通过这种机制导致胰岛素抵抗并增加糖尿病风险。
