Ciofetta M, Lalli C, Del Sindaco P, Torlone E, Pampanelli S, Mauro L, Chiara D L, Brunetti P, Bolli G B
Dipartimento di Medicina Interna e Scienze Endocrine e Metaboliche, Università di Perugia, Italy.
Diabetes Care. 1999 May;22(5):795-800. doi: 10.2337/diacare.22.5.795.
To quantitate the contribution of postprandial blood glucose, which improves with the short-acting insulin analog lispro [Lys(B28),Pro(B29)] in type 1 diabetes, to the overall 24-h blood glucose concentration and the long-term HbA1c concentration under conditions of different postabsorptive blood glucose.
A total of 24 type 1 diabetic patients on long-term intensive therapy with premeal human regular insulin (Hum-R) and bedtime NPH were randomly assigned to a continuation of Hum-R (group 1, n = 8), lispro (group 2, n = 8), or lispro + NPH (in variable proportions) administered at mealtime (group 3, n = 8) for 3 months, NPH administered at bedtime was continued in all three groups. Data from home blood glucose monitoring were collected, and a 24-h plasma glucose and insulin profile was obtained during a 2-day hospital visit to calculate areas under the postprandial glucose curve (3.5 h after breakfast, 3.5 h after lunch, and 3.0 h after dinner for a total of 10.0 h) and the postabsorptive blood glucose curve (the remaining 14.0 h out of 24.0 h) (AUC). Eight nondiabetic subjects were also studied.
The substitution of Hum-R with lispro (group 2) resulted in lower postprandial blood glucose, but greater postabsorptive blood glucose (P < 0.05 vs. group 1). The postprandial blood glucose AUC was lower (161 +/- 19 vs. 167 +/- 20 mg.100 ml-1.h-1), but the postabsorptive blood glucose AUC was greater (155 +/- 22 vs. 142 +/- 19 mg.100 ml-1.h-1) (P < 0.05). Therefore, the 24-h blood glucose AUC was no different (NS). Consequently, HbA1c was no different (NS). This occurred because in group 2, mealtime lispro resulted in normal prandial plasma insulin, but also resulted in lower interprandial concentration (P < 0.05 vs. group 1). When NPH was added to lispro (30% at breakfast, 40% at lunch, 10% at dinner) in group 3, postabsorptive plasma insulin was similar to group 1 (NS), in group 3, the postprandial blood glucose AUC (153 +/- 17 mg.100 ml-1.h-1) was lower and the postabsorptive blood glucose AUC was no different, as compared with group 1 (NS). Therefore, the 24-h blood glucose AUC was lower (147 +/- 17 vs. 155 +/- 21 and 158 +/- 20 mg.100 ml-1.h-1), and HbA1c was lower (6.41 +/- 0.12 vs. 6.84 +/- 0.2 and 6.96 +/- 0.2% (groups 3, 1, and 2 respectively, P < 0.05). Frequency of hypoglycemia was greater in group 2 (P < 0.05), but not in group 3 (NS) vs. group 1.
在不同空腹血糖条件下,定量评估1型糖尿病患者餐后血糖对整体24小时血糖浓度及长期糖化血红蛋白(HbA1c)浓度的贡献,短效胰岛素类似物赖脯胰岛素[赖氨酰(B28),脯氨酰(B29)]可改善餐后血糖。
24例接受餐前人常规胰岛素(Hum-R)和睡前中性鱼精蛋白锌胰岛素(NPH)长期强化治疗的1型糖尿病患者,随机分为继续使用Hum-R组(第1组,n = 8)、赖脯胰岛素组(第2组,n = 8)或餐时使用不同比例赖脯胰岛素+NPH组(第3组,n = 8),为期3个月,所有三组均继续睡前注射NPH。收集家庭血糖监测数据,并在住院2天期间获取24小时血浆葡萄糖和胰岛素谱,以计算餐后血糖曲线下面积(早餐后3.5小时、午餐后3.5小时和晚餐后3.0小时,共10.0小时)和空腹血糖曲线下面积(24.0小时中的其余14.0小时)(AUC)。还研究了8名非糖尿病受试者。
用赖脯胰岛素替代Hum-R(第2组)导致餐后血糖降低,但空腹血糖升高(与第1组相比,P < 0.05)。餐后血糖AUC较低(161±19 vs. 167±20 mg·100 ml-1·h-1),但空腹血糖AUC较高(155±22 vs. 142±19 mg·100 ml-1·h-1)(P < 0.05)。因此,24小时血糖AUC无差异(无显著性差异)。相应地,HbA1c也无差异(无显著性差异)。这是因为在第2组中,餐时使用赖脯胰岛素使餐时血浆胰岛素正常,但也导致餐间浓度降低(与第1组相比,P < 0.05)。当在第3组中赖脯胰岛素添加NPH(早餐时30%,午餐时40%,晚餐时10%)时,空腹血浆胰岛素与第1组相似(无显著性差异),在第3组中,餐后血糖AUC(153±17 mg·100 ml-1·h-1)较低,空腹血糖AUC与第1组无差异(无显著性差异)。因此,24小时血糖AUC较低(147±17 vs. 155±21和158±20 mg·100 ml-1·h-1),HbA1c较低(6.41±0.12 vs. 6.84±0.2和6.96±0.2%,分别为第3组、第1组和第2组,P < 0.05)。第2组低血糖发生频率较高(P < 0.05),但第3组与第1组相比无差异(无显著性差异)。