摘要目的 探讨慢性阻塞性肺疾病(慢阻肺)患者血清分泌型卷曲相关蛋白5(sfrp5)水平与气道炎症和胰岛素抵抗的关系.方法 选取2015年2月至2017年1月门诊慢阻肺患者178例,其中男152例,女64例,同期健康体检者纳入为对照组99名,其中男87名,女41名.对比两组血清sfrp5水平,观察患者稳态模型评估的胰岛素抵抗指数(HOMA-IR),分为胰岛素抵抗慢阻肺组(HOMA-IR≥2.29)、非胰岛素抵抗慢阻肺组、单纯性胰岛素抵抗组和正常对照组各亚组的血清sfrp5及诱导痰炎症因子水平.结果 慢阻肺组的sfrp5水平显著高于健康对照组(t=-14.29,P<0.001);胰岛素抵抗慢阻肺组sfrp5水平[(8±3)ng/ml]显著低于非胰岛素抵抗慢阻肺组[(10±5)ng/ml]、单纯性胰岛素抵抗组[(13±3)ng/ml]、正常对照组[(14±4)ng/ml,F=35.85,P<0.01].胰岛素抵抗慢阻肺组的In(HOMA-IR)、诱导痰肿瘤坏死因子-α(TNF-α)、IL-6水平高于非胰岛素抵抗慢阻肺组、单纯胰岛素抵抗组和正常对照组(F值分别为64.968、41.40、64.15,均P<0.01);非胰岛素抵抗慢阻肺组的In(HOMA-IR)、诱导痰TNF-α、IL-6水平显著高于单纯胰岛素抵抗组、正常对照组;胰岛素抵抗慢阻肺组FEV1/FVC、FEV1占预计值显著低于非胰岛素抵抗慢阻肺组、单纯性胰岛素抵抗组、正常对照组(F值分别为2.481、8.37,均P<0.05);非胰岛素抵抗慢阻肺组的FEV1/FVC、FEV1占预计值%显著低于正常对照组和单纯性胰岛素抵抗组;血清sfrp5水平与FEV1/FVC、FEV1占预计值%呈正比(r值分别为0.466、0.412,均P<0.01),与In(HOMA-IR)、诱导痰TNF-α、IL-6呈反比(r值分别为-0.304、-0.459、-0.517,均P<0.01).体重指数、In(HOMA-IR)和诱导痰IL-6为血清sfrp5的独立相关因素(r2值分别为0.286、0.176、14.69,均P<0.01).结论 sfrp5可能同时与慢阻肺、胰岛素抵抗有关;胰岛素抵抗可能与气道炎症、气流受限有关;sfrp5可能参与慢阻肺的发生发展,也可能是胰岛素抵抗影响气道炎症的关键环节.

abstractsObjective To investigate the relationship between serum secreted frizzled-related protein 5(sfrp5) levels, insulin resistance, and airway inflammation in patients with chronic obstructive pulmonary disease(COPD).Method A total of 178 COPD patients visiting our respiratory outpatient clinic from February 2015 to January 2017 were enrolled , and 99 healthy control subjects from the same time period were selected .Serum sfrp5 levels were compared between the 2 groups.Serum sfrp5 and inflammatory cytokines in induced sputum were observed in the 4 subgroups:insulin resistant COPD group [ homeostasis model assessment of insulin resistance (HOMA-IR)≥2.29], non-insulin resistant COPD group, non-COPD insulin resistant group , and healthy control group . Results Serum sfrp5 levels were found to be significantly higher in the COPD group as compared to the healthy control group ( t=-14.29, P<0.001). Serum sfrp5 levels in the insulin resistant COPD group [(8 ±3)ng/ml] were significantly lower than that of the non-insulin resistant COPD group [(10 ±5)ng/ml], non-COPD insulin resistant group [(13 ±3)ng/ml], and normal control group [(14 ±4)ng/ml, F=35.85, P<0.01].The insulin resistant COPD group had higher levels of In(Homa-IR), as well as tumor necrosis factor-α(TNF-α) and interleukin-6 (IL-6) in induced sputum as compared to the non-insulin resistant COPD group , non-COPD insulin resistant group , and healthy control group ( F values were 64.968, 41.40, 64.15, respectively, P value <0.01 for all items).The non-insulin resistant COPD group had higher levels of In (HOMA-IR) as well as TNF-αand IL-6 in induced sputum as compared to the non-COPD insulin resistant group and healthy control group .FEV1/FVC and FEV1%predicted were significantly lower in the insulin resistant COPD group as compared to those of non-insulin resistant COPD group and non-COPD insulin resistant group , and healthy control group ( F values were 2.481 and 8.37, respectively, P value <0.05 for all items ) .FEV1/FVC and FEV1%predicted were significantly lower in the non-insulin resistant COPD group as compared to those of the healthy control group and non-COPD insulin-resistant group.Serum sfrp5 levels were positively correlated to FEV 1/FVC and FEV1 predicted ( r values were 0.466 and 0.412, respectively; P values were <0.001 and 0.007, respectively) and inversely correlated to In ( HOMA-IR) and TNF-αand IL-6 in induced sputum (r values were -0.304, -0.459, -0.517, respectively; P values were <0.001, 0.002, <0.001, respectively) .BMI, ln ( HOMA-IR), and IL-6 in induced sputum were independent related factors (r2 values were 0.286, 0.176, 14.69, respectively; P values were <0.01 for all items) Conclusion Sfrp5 may be concurrently associated with COPD and insulin resistance;insulin resistance may be associated with airway inflammation and airflow limitation .Sfrp5 may be involved in the development of COPD and may be the key link by which insulin resistance exerts its effects on airway inflammation.