罗格列酮与胰岛素治疗对2型糖尿病患者胰岛β细胞第一时相分泌功能的影响

目的罗格列酮（RGZ）与胰岛素治疗对2型糖尿病（T2DM）患者胰岛功能的影响。方法FPG）11．1mmol／L的患者随机分为胰岛素治疗（Ins）组和胰岛素＋罗格列酮治疗（Ins＋RGZ）组，两组年龄、病程、BMI均无统计学差异。血糖达标后再维持治疗3个月。治疗前后均作静脉糖耐量试验（IVGTT），比较两组糖代谢和胰岛功能的变化。结果治疗后的FPG、2hPG、HbA1c、静脉葡萄糖曲线下面积（AUC-G0～60）均显著下降，HOMA—B改善（P〈0．01或P〈0．05），两组间无统计学差异。两组IVGTT10min内胰岛素释放曲线下面积／60min内胰岛素释放曲线下面积（AUC-I0～10／AUC-I0～60）分别增加10％和12％（P=0．085，0．05）。Ins＋RGZ组I2、I5、I10及FC-P显著提高，Ins组增高无统计学意义。逐步回归分析显示，治疗后FPG和2hPG下降与负荷后胰岛素增值和血糖增值比值呈正相关（r=0．593，P=0．000；r=0．548，P=0．001），表明治疗后胰岛素处理葡萄糖能力与血糖控制程度呈正相关。结论罗格列酮（而不是胰岛素）能恢复第一时相胰岛素分泌。T2DM患者早期联用RGZ，有利于保护胰岛β细胞功能。

Effect of rosiglitazone versus insulin on the first phase insulin secretion of islet β cell in type 2 diabetes patients

Objective To investigate the effect of rosiglitazone versus insulin on pancreatic 13 cell function in type 2 diabetic patients. Methods Type 2 diabetic patients with severe hyperglycaemia （FPG 〉11. lmmol/L） were assigned randomly to receive insulin versus insulin combined with rosiglitazone treatment for 3 months. At baseline and at 3 months, the fasting and postprandial plasma glucose, and the levels of glucose, insulin and C-peptide one hour after intravenous glucose tolerance test were determined. Results The two groups were well matched for age, duration of diabetes, and BMI. After three months of treatment there was significant decrease in fasting plasma glucose, postprandial plasma glucose, HbA1 c and area under the curve of glucose, as well as HOMA-β improvement（all P〉0.05）, but there was no significant difference between the two groups（P〉0. 05）. The ratio of AUCI0-10/AUCI0-60 was increased by 10% and 12% in two groups respectively（P=0. 085, 0.05）. Only in the rosiglitazone group was there a significant improvement in acute insulin response to glucose and in C peptide in IVGTT at 10 minutes. The linear stepwise regression analysis showed that the decrease of FPG and 2hPG after therapy positively correlated with the increase of △ Insulin/△ Glucose during IVGTT （r= 0. 593, P = 0. 000 ; r= 0. 548, P = 0. 001）. Conclusions Rosiglitazone, but not insulin, induces a recovery of pancreatic β cell function, which is evidenced by the restoration of the first-phase insulin response to glucose in type 2 diabetes.