冠心病患者胰岛素抵抗及胰岛β细胞功能检测临床意义的研究  

Insulin Resistance and the Function of Pancreatic β-cell in Patients With Prior Coronary Heart Disease and Normal Fasting Plasm Glucose

作　　者：孙伟霞[1] 杨萍[1] 周雪艳[1] 

机构地区：[1]吉林大学中日联谊医院心内科,吉林省长春市130012

出　　处：《中国循环杂志》2007年第5期347-350,共4页Chinese Circulation Journal

基　　金：吉林省科技厅基础处项目(200505173)

摘　　要：目的:通过口服葡萄糖耐量试验研究空腹血糖正常的冠心病患者胰岛素抵抗状态、胰岛β细胞分泌功能及其临床意义。方法:对冠心病组(35例)及对照组(30例)按空腹及服糖后30、60、120和180min进行糖耐量、胰岛素释放实验,测量各时点血糖值及胰岛素值。同时测量其血压、身高、体重、总胆固醇、甘油三酯,并计算出体重指数(BMI)=体重(kg)/身高2(m2)。按照稳态模型胰岛素抵抗指数(HOMA-IR)=空腹胰岛素(FINS)×空腹血糖(FPG)/22.5;胰岛β细胞分泌指数(HBCI)=20×空腹胰岛素/(空腹血糖-3.5);早期胰岛素分泌指数(△I30/△G30)=口服葡萄糖耐量试验30min胰岛素增量与葡萄糖增量的比值;李氏β细胞胰岛素分泌指数(MBCI)=(空腹胰岛素×空腹血糖)/(血糖2h+血糖1h-2×空腹血糖)公式计算稳态模型胰岛素抵抗指数、胰岛β细胞分泌指数、△I30/△G30及李氏β细胞胰岛素分泌指数值。结果:空腹血糖正常的冠心病患者糖代谢异常(120min血糖≥7.8mmol/L)的发生率为43%,明显高于对照组23%,仅用空腹血糖这些患者将不能被诊断;冠心病组空腹及服糖后120min、180min胰岛素水平、稳态模型胰岛素抵抗指数显著高于对照组[(11.4±9.4)vs(5.3±3.1)mU/L,(71.6±48.5)vs(31.2±22.0)mU/L,(42.7±35.4)vs(8.6±6.9)mU/L,(0.62±0.32)vs(0.47±0.21),P<0.01],△I30/△G30、李氏β细胞胰岛素分泌指数低于对照组[(1.13±0.65)vs(1.42±0.57),(1.03±0.35)vs(1.36±0.37),P<0.01],差异有显著性;Logistic回归分析显示稳态模型胰岛素抵抗指数、120min胰岛素水平、总胆固醇与冠心病的发生显著相关(OR值分别为1.432、0.644、1.116,P<0.05)。结论:空腹血糖正常的冠心病患者糖代谢异常发病率明显高于对照组,简易口服葡萄糖耐量试验可揭示血糖代谢状态,应常规用于冠心病患者血糖代谢异常的诊断。冠心病患者存在胰岛素抵抗及胰岛β细胞分泌功能缺陷。Objective ： To explore the prevalence of abnormal glucose regulation, the function of pancreatic β-cell and insulin resistance （IR） in patients with coronary heart disease （CHD） and normal fasting plasm glucose（FPG）. Methods： Seventy five gram oral glucose tolerance testing （OG337） was performed in 35 patients with CHD and 30 normal controls. Plasma glucose and insulin after OGTT were measured at O, 30, 60, 120 and 180 minutes and body height/weight ,blood pressure,blood lipids （TC,TG） were measured. Insulin secretion and insulin resistance were evaluated. The early insulin secretion index （Δ130/ΔG30, HOMA-IR = FINS × FPG/22. 5 ）, HOMA-β cell index （ HBCI = 20 × FINS/（ FPG - 3.5 ） ） ; and Li＇s new β cell insulin secretion index（ MBCI = （FINS × FPG）/（ PG2h ＋ PG1 h-2FPG））were calculated. Results：In patients with CHD and normal FPG, 43% had abnormal glucose regulation （2-h postload blood glucose ≥7.8 mmol/L） higher than those of controls （23%）. By FPG, abnormal glucose in these patients were not found. Insulin at 0,120,180 minutes and HOMA-IR in patients with CHD was higher than that of controls（ 11.4 ±9.4 vs 5.3 ± 3. 1 mU/L,71.6 ±48. 5 vs 31.2±22. 0 mU/L,42. 7±35.4 vs 8. 6±6. 9 mU/L,0. 63 ±0. 32 vs 0. 47 ±0. 21 ;P 〈0. 01 ）. ΔI30/ΔG30, MBCI were lower than those of controls （ 1. 13 ± 0, 65 vs 1.42 ± 0. 57,1.03 ± 0. 35 vs 1. 36 ± 0. 37 ; P 〈 0. 01 ）. Logistic regression analysis revealed that insulin at 120 minutes, HOMA-IR and TC were positively correlated with the development of CHD （OR 1. 432,0. 644 and 1.116, respectively, P 〈 0. 05 ）. Conclusions：Abnormal glucose in patients with CHD and normal FPG is higher than that of controls. OGTT is a feasible tool to disclose glucometabolic status and it should be included in the diagnostic routine examinations of such patients. There exist IR and dysfunction of pancreatic β-cell in patients with CHD.

关 键 词：冠心病 糖代谢异常 胰岛素抵抗 胰岛Β细胞功能 

分 类 号：R541.4[医药卫生—心血管疾病]