CAJ | 학술논문

目的观察阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者血清解耦联蛋白-2(UCP-2)的变化,探讨OSAHS并发糖代谢异常的可能机制.方法选取单纯OSAHS患者31例,轻、中度组16例,重度组15例；OSAHS合并2型糖尿病患者14例；单纯2型糖尿病患者14例及单纯肥胖者18例；均行整夜多导睡眠监测(PSG)及空腹血糖(FPG)、糖化血红蛋白(HbA1c)测定,ELISA法检测血清中UCP-2水平,了解UCP-2在OSAHS患者糖代谢变化中发挥的作用.结果与单纯肥胖对照组相比,糖尿病组、重度OSAHS组、合并组UCP-2水平明显升高(P＜0.05),合并组较糖尿病组与重度组UCP-2升高更为明显(P＜0.05).UCP-2水平与AHI、HbA1c、FPG呈正相关(r=0.795、0.513、0.268,P值均＜0.05),与LSO2呈负相关(r=-0.721,P＜0.05).结论 OSAHS可引起UCP-2的血清水平升高,其可能在OSAHS致糖代谢异常中起重要作用.
목적 관찰조새성수면호흡잠정저통기종합정(OSAHS)환자혈청해우련단백-2(UCP-2)적변화,탐토OSAHS병발당대사이상적가능궤제.방법 선취단순OSAHS환자31례,경、중도조16례,중도조15례；OSAHS합병2형당뇨병환자14례；단순2형당뇨병환자14례급단순비반자18례；균행정야다도수면감측(PSG)급공복혈당(FPG)、당화혈홍단백(HbA1c)측정,ELISA법검측혈청중UCP-2수평,료해UCP-2재OSAHS환자당대사변화중발휘적작용.결과 여단순비반대조조상비,당뇨병조、중도OSAHS조、합병조UCP-2수평명현승고(P＜0.05),합병조교당뇨병조여중도조UCP-2승고경위명현(P＜0.05).UCP-2수평여AHI、HbA1c、FPG정정상관(r=0.795、0.513、0.268,P치균＜0.05),여LSO2정부상관(r=-0.721,P＜0.05).결론 OSAHS가인기UCP-2적혈청수평승고,기가능재OSAHS치당대사이상중기중요작용.
Objective To observe the disorder of glucose mechanism and the changes of serum uncoupling protein-2 (UCP-2) levels in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS) and explore the morbidity mechanism of glucose metabolism disorder caused by OSAHS.Methods To select 31 patients with OSAHS,these patients were divided into mild to moderate group (16 cases) and severe group (15 cases).To select 14 OSAHS patients with type 2 diabetes,14 patients with type 2 diabetes and 18 simple obesity patients.All patients received PSG all night and H bA1c,fasting plasma glucose (FPG) level were measured.UCP-2 level were tested by enzyme-linked immunosorbent assay (ELISA).To understand the changes of UCP-2 levels with OSAHS.Results Compared with the control group,the levels of UCP-2 in severe group,the OSAHS patients with type 2 diabetes group and the simple type 2 diabetes group obviously elevated.The UCP-2 level in the OSAHS patients with type 2 diabetes group was significantly higher than that in the simple type 2 diabetes group and sever group.UCP-2 is positively related to AHI,HbA1c,FPG (r =0.795,0.513,0.268,P ＜ 0.05),and negatively related to LSaO2 (r =-0.721,P ＜0.05).Conclusions OSAHS induced the increased expression of UCP-2.It indicated that UCP-2 may play a important role in the development of glucose metabolism disorder caused by OSAHS.