Division of Cardiology, Department of Internal Medicine, Buddhist Tzu Chi General Hospital, Taipei Branch, Xindian City, Taipei, Taiwan.
Metabolism. 2010 Jun;59(6):824-30. doi: 10.1016/j.metabol.2009.09.030. Epub 2009 Dec 9.
Insulin resistance, which plays a fundamental role in the pathogenesis of metabolic syndrome and type 2 diabetes mellitus, is associated with serum levels of inflammatory markers and abdominal obesity. Whether insulin resistance is caused by inflammation or is an epiphenomenon of obesity remains unresolved. We therefore conducted a cross-sectional study to investigate whether the association between insulin resistance and C-reactive protein (CRP) levels is independent of abdominal obesity in a nondiabetic Taiwanese population. The study included 574 Taiwanese participants (300 men and 274 women) who were nondiabetic persons with CRP levels not exceeding 10 mg/L and who did not have a history of cardiovascular disease or were taking medication for dyslipidemia. All participants were of Han-Chinese origin. The degree of insulin resistance was determined using the homeostasis model assessment of insulin resistance (HOMA-IR). The CRP levels were categorized into quartiles from the lowest to the highest concentrations (Q1-Q4). Blood pressure, fasting glucose level, triglycerides level, waist circumference, and HOMA-IR were all found to be significantly higher in Q3 and Q4 than in Q1 and Q2. Stratified analysis by sex and abdominal obesity showed that HOMA-IR was significantly associated with CRP levels in both sexes in either obese or nonobese populations. Multiple linear regression analysis adjusting for age, smoking, components of metabolic syndrome, and waist circumference showed that the association between HOMA-IR and CRP levels remained significant in both men and women (P = .029 for men and P < .001 for women). These findings confirm that insulin resistance is strongly associated with CRP levels independent of abdominal obesity in nondiabetic Taiwanese. Factors other than abdominal obesity, such as polymorphisms in the CRP gene, may influence the association of insulin resistance with CRP levels in different ethnic populations.
胰岛素抵抗在代谢综合征和 2 型糖尿病的发病机制中起着根本作用，与血清炎症标志物和腹部肥胖有关。胰岛素抵抗是由炎症引起的，还是肥胖的继发现象，目前仍未解决。因此，我们进行了一项横断面研究，以调查在非糖尿病的台湾人群中，胰岛素抵抗与 C 反应蛋白（CRP）水平之间的关联是否独立于腹部肥胖。该研究纳入了 574 名台湾参与者（300 名男性和 274 名女性），他们是非糖尿病患者，CRP 水平不超过 10mg/L，且无心血管疾病史或正在服用调脂药物。所有参与者均为汉族人。采用稳态模型评估胰岛素抵抗（HOMA-IR）来确定胰岛素抵抗的程度。将 CRP 水平从最低到最高浓度分为四等份（Q1-Q4）。结果显示，Q3 和 Q4 的血压、空腹血糖水平、甘油三酯水平、腰围和 HOMA-IR 均显著高于 Q1 和 Q2。按性别和腹部肥胖分层分析显示，在肥胖和非肥胖人群中，HOMA-IR 与 CRP 水平在两性中均显著相关。经年龄、吸烟、代谢综合征成分和腰围校正的多元线性回归分析显示，HOMA-IR 与 CRP 水平之间的关联在男性和女性中均保持显著（男性 P =.029，女性 P <.001）。这些发现证实，在非糖尿病的台湾人中，胰岛素抵抗与 CRP 水平密切相关，与腹部肥胖无关。除了腹部肥胖之外，CRP 基因的多态性等因素可能会影响不同种族人群中胰岛素抵抗与 CRP 水平之间的关联。
