Centre for Precision Health, Edith Cowan University School of Medical and Health Sciences, Room 521, Building 21/270 Joondalup Drive, Perth, WA, 6027, Australia.
Department of Pediatrics, Second Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong, China.
Cardiovasc Diabetol. 2023 Dec 20;22(1):351. doi: 10.1186/s12933-023-02067-0.
Adiposity and elevated inflammation are two hallmarks of hyperglycemia. However, it is unknown whether clustering of elevated inflammation and adiposity interact act on diabetogenesis and lead to a greater risk for incident type 2 diabetes (T2D).
Adiposity was indicated by body mass index, waist circumference and ultrasonography-measured fatty liver degrees. Elevated inflammation was indicated as high-sensitivity C-reactive protein levels ≥ 2 mg/L. Time-to-event survival analyses were conducted to investigate the joint effect of adiposity and inflammation on incident T2D on both multiplicative and additive scales.
Among 82,172 non-diabetic participants from a prospective cohort in China, 14,278 T2D occurred over a median follow-up of 11 years. In the multivariable-adjusted model, elevated inflammation [1.12 (1.08‒1.16)] and adiposity [1.76 (1.69‒1.83) for overweight/obesity, 1.49 (1.44‒1.55) for central obesity, and 2.02 (1.95‒2.09) for fatty liver] were significantly associated with incident diabetes. Higher adiposity-associated risks and incidence rates of diabetes were observed with elevated inflammation. When studying the joint effect, the adjusted HRs were 1.77 (1.69‒1.85) for overweight/obesity, 1.14 (1.06‒1.23) for elevated inflammation, and 2.08 (1.97‒2.19) for their joint effect, with a relative excess risk due to interaction of 0.17 (0.05‒0.28). The attributable proportions were 71.30% for overweight/obesity, 12.96% for elevated inflammation, and 15.74% for their interaction. Similar results were observed when adiposity was assessed as waist circumference or fatty liver.
Adiposity and elevated inflammation synergically lead to greater risks of incident diabetes than addition of each individual exposure. Strategies simultaneously targeting both risks should produce more benefits for diabetes prevention than through initiatives directed at each separate risk.
肥胖和炎症升高是高血糖的两个标志。然而，尚不清楚炎症升高和肥胖的聚集是否会相互作用影响糖尿病的发生，并导致 2 型糖尿病（T2D）发病风险增加。
肥胖程度由体重指数、腰围和超声测量的脂肪肝程度来表示。炎症升高表示高敏 C 反应蛋白水平≥2mg/L。采用时间事件生存分析来研究肥胖和炎症对中国前瞻性队列中 82172 名非糖尿病参与者发生 T2D 的联合作用，分别在相乘和相加尺度上进行分析。
在中位随访 11 年期间，共发生了 14278 例 T2D。在多变量调整模型中，炎症升高[1.12（1.08-1.16）]和肥胖[超重/肥胖症为 1.76（1.69-1.83），中心性肥胖为 1.49（1.44-1.55），脂肪肝为 2.02（1.95-2.09）]与糖尿病发病显著相关。炎症升高时，肥胖相关的风险和糖尿病发病率更高。在研究联合效应时，超重/肥胖的调整 HR 为 1.77（1.69-1.85），炎症升高的 HR 为 1.14（1.06-1.23），两者联合作用的 HR 为 2.08（1.97-2.19），交互作用所致的相对超额风险为 0.17（0.05-0.28）。超重/肥胖的归因比例为 71.30%，炎症升高的归因比例为 12.96%，两者相互作用的归因比例为 15.74%。当使用腰围或脂肪肝来评估肥胖时，得到了相似的结果。
肥胖和炎症升高协同作用导致发生糖尿病的风险高于每个单独暴露因素的风险相加。同时针对这两种风险的策略应比针对每种单独风险的措施能带来更大的糖尿病预防效益。
