胰岛素强化治疗对初诊2型糖尿病患者血清Chemerin的影响

Influence of intensive insulin therapy on serum Chemerin in newly diagnosed type 2 diabetes

目的观察初诊2型糖尿病(T2DM)患者胰岛素强化治疗对血清趋化素(Chemerin)、超敏C反应蛋白(hs-CRP)、胰岛素抵抗指数(HOMA-IR)等的影响。方法选择60例初诊T2DM患者随机分为强化组和对照组,分别进行胰岛素强化和口服药物治疗4周,治疗前后检测血清Chemerin、hs-CRP,同时检测血糖、血脂、胰岛素。结果 (1)强化组及对照组空腹血糖(FPG)、餐后2 h血糖(2h PG)、甘油三酯(TG)、总胆固醇(TC)、hs-CRP治疗后均较治疗前下降(P<0.05)。强化组治疗后FPG、2h PG、hs-CRP较对照组下降(P<0.05)。(2)强化组空腹胰岛素(FINS)、餐后2 h胰岛素(PINS)、胰岛β细胞功能指数(HOMA-β)治疗后较治疗前增高,而HOMA-IR、Chemerin下降(P<0.05);对照组PINS、HOMA-β治疗后较治疗前增高,而HOMA-IR下降(P<0.05)。强化组治疗后PINS、HOMA-β较对照组增高,而HOMA-IR、Chemerin下降(P<0.05)。结论胰岛素强化治疗能减轻炎症,改善胰岛素抵抗,Chemerin在2型糖尿病的亚临床炎症、胰岛素抵抗的病理机制中可能具有重要作用。

Objective To investigate the influence of intensive insulin therapy on serum chemerin,hs- CRP and HOMA- IR in newly diagnosed patients with type 2 diabetes mellitus. Methods Sixty type 2 diabetic subjects were divided into intensive and control group randomly,which were respectively received intensive insulin therapy and oral hypoglycemic agents for 4 weeks.Serum chemerin,hs- CRP,blood glucose,lipids and insulin concentrations were measured before and after therapy. Results A. Levels of FPG,2h PG,TG,TC and hs- CRP after therapy were lower than those before therapy in both intensive and control group（ P〈 0. 05）. Levels of FPG,2h PG and hs- CRP in intensive group after therapy were lower than those in control group（ P〈 0. 05）. B. In intensive group,increased levels of FINS,PINS,HOMA- β and decreased levels of HOMA- IR,chemerin after treatment were observed compared with those before treatment（ P〈 0. 05）. In control group,increased levels of PINS,HOMA- β and decreased levels of HOMA- IR after treatment were observed compared with those before treatment（ P〈 0. 05）.Levels of PINS and HOMA- β in intensive group after therapy increased compared with those in control group,whereas levels of HOMA- IR and chemerin decreased（ P〈 0. 05）. Conclusion Intensive insulin therapy could alleviate inflammation and insulin resistance. Chemerin may play an important role in the pathophysiology of subclinical inflammation and insulin resistance in type2 diabetes mellitus.