血清抵抗素、超敏C反应蛋白与2型糖尿病患者体成分之间的关系

目的观察血清抵抗素及超敏C反应蛋白（hs—CRP）在肥胖、非肥胖2型糖尿病患者中的含量，分析与骨密度（BMD）、体脂成分之间的关系。方法入选病例分3组：正常对照组28例、糖尿病非肥胖组30例、糖尿病肥胖组30例。采用酶联免疫测定法检测空腹血清抵抗素，免疫比浊法测定血清hs—CRP，双能X线骨密度仪（DXA）检测各部位BMD、体内脂肪百分比。通过检测空腹血糖（FPG）与空腹胰岛素（FINS），计算胰岛素分泌功能指数（HOMA2-％B）、胰岛素敏感性指数（HOMA2-％S）以及胰岛素抵抗指数（HOMA2-IR）。结果糖尿病非肥胖组hs—CRP、抵抗素较正常对照组显著升高（2．34±0．75）mg／L比（1．98±2．24）mg／L；（20．19±11．20）μg/L比（15．59±11．10）μg／L，均P〈0．05]，糖尿病肥胖组hs—CRP（4．94±2．35）mg／L]、抵抗素（25．83±9．56）μg／L】较正常对照组显著升高（P〈0．01），亦高于糖尿病非肥胖组（P〈0．01）。相关分析显示：抵抗素与BMI存在负相关（r=-0．252，P〈0．05），与hs—CRP、HOMA2-％B、HOMA2-IR存在正相关（r分别为0．563、0．225、0．667，均P〈0．05），而与各部位BMD无相关性。hs—CRP与腰围（WC）、体重指数（BMI）、HOMA2-IR、上肢脂肪百分比、大腿脂肪百分比、躯干脂肪百分比、全身脂肪百分比存在相关性（r分别为0．773、0．594、0．662、0．540、0．557、0．530、0．561，均P〈0．01），与抵抗素、躯干BMD存在相关性（r分别为0．563、0．224，均P〈0．05）。校正年龄、空腹血糖等因素之后，hs—CRP仍与WC、BMI、HOMA2-IR、抵抗素和大腿脂肪百分比％独立相关。结论抵抗素与HOMA2-％B、HOMA2-IR相关，表明其在糖尿病发病机制中起重要作用。hs—CRP是已知的炎症因子．hs—CRP与抵抗素的紧密联系提示抵抗素也可能是炎症因子之一。中心性肥胖可能是导致CRP、抵抗素升高的重要原因之一，炎症和（或）肥胖是胰岛素抵抗、2型糖尿病发生的一个启动因子。

Relationships between serum resistin, hs-CRP and body compositions in type 2 diabetes mellitus with and without obesity

Objective To investigate serum resistin, high-sensitivity C-reactive protein （hs-CRP）, bone mineral density （BMD）, body compositions and the relationships among them in normal controls, type 2 diabetes mellitus （DM） patients with and without obesity. Methods The subjects were divided into 3 groups： normal control group （n = 28）, type 2 DM without obesity group （n = 30）, type 2 DM with obesity group （n = 30）. The serum resistin was measured by enzyme immunoassay, hs-CRP was measured by immunoturbidimetry. The bone mineral density （BMD） and body compositions were measured by dual-energy X-ray absorptiometry （DXA）. Homeostasis model was used to assess β-cell function （HOMA2-%B）, insulin resistance index （HOMA2-IR） and insulin sensitivity index （HOMA2-%S）. Results The serum resistin and hs-CRP levels in type 2 DM without obesity group were higher than that in the normal control group （20.19±11.2） mg/L vs （15.59±11.10） mg/L, （2.34±0.75） μg/L vs （1.98±2.24）μg/L, all P 〈 0.05], and the index in type 2 DM with obesity group were higher than those in the normal con-trol group and in DM without obesity group （25.83±9.56） μg/L vs （20.19±11.20） μg/L, （4.94±2.35） mg/L vs （2.34±0.75） rag/L, all P 〈 0.01]. Pearson analysis showed that the serum resistin concentration was correlated with BMI, hs-CRP, HOMA2-%B, HOMA2-IR （r = -0.252, 0.563, 0.225, 0.667, all P 〈 0.05）, while had no correlation with BMD. hs-CRP was correlated with WC, BMI, HOMA2-Ir, arms fat percent）, legs fat percent, trunk fat percent, total fat percent （r = 0.773, 0.594, 0.662, 0.540, 0.557, 0.530, 0.561, all P 〈 0.01）, and also correlated with resistin, trunk BMD （r = 0.563, 0.224, all P 〈 0.05）. After adjusting of age and plasma glucose, hs-CRP was still correlated to WC, BMI, HOMA2-IR, resistin and legs fat per-cent. Conclusion The resistin has correlation with HOMA2-%B, HOMA2-IR, it plays an important role in the development of diabetes, hs-CRP is a known inflammation faetor, the closed relationship between hs-CRP and resistin suggests that resistin can also be an inflammation factor. The sources of resistinand hs-CRP in type 2 DM without obesity can be central fat because of the higher WHR in this group. Inflammation and （or） obesity maybe an activate factor in insulin resistance and type 2 diabetes.