Impact of pramlintide on glucose fluctuations and postprandial glucose, glucagon, and triglyceride excursions among patients with type 1 diabetes intensively treated with insulin pumps

被引:99
作者
Levetan, C
Want, LL
Weyer, C
Strobel, SA
Crean, J
Wang, Y
Maggs, DG
Kolterman, OG
Chandran, M
Mudaliar, SR
Henry, RR
机构
[1] MedStar Clin Res Ctr, Washington, DC 20003 USA
[2] Amylin Pharmaceut, San Diego, CA USA
[3] Univ Calif San Diego, Vet Affairs Med Ctr, San Diego Healthcare Syst, San Diego, CA 92161 USA
关键词
D O I
10.2337/diacare.26.1.1
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
OBJECTIVE - To assess the effects of adjunctive treatment with pramlintide, an analog of the beta-cell hormone amylin, on 24-h glucose fluctuations and postprandial glucose, glucagon, and triglyceride excursions in patients with type I diabetes intensively treated with Continuous subcutaneous insulin infusion (CSII). RESEARCH DESIGN AND METHODS - in this study, 18 patients (16 of whom could be evaluated) with type 1 diabetes (age 44 +/- 11 years, HbA(1c) 8.2 +/- 1.3% [mean SD]) were given mealtime injections of 30 mug pramlintide t.i.d. for 4 weeks in addition to their preexisting CSII regimen (16 lispro, 2 regular insulin). Mealtime insulin boluses were reduced by a minimum of 10% during the first 3 days, and re-adjusted thereafter based on clinical judgment. At weeks 0 (baseline), 4 (on treatment), and 6 (2 weeks off treatment), 24-h interstitial glucose concentrations were measured using a continuous glucose monitoring system (CGMS), and postprandial plasma glucose, glucagon, and triglyceride concentrations were measured in response to a standardized test meal. RESULTS - At baseline, patients had excessive 24-h glucose fluctuations, with 59% of the CGMS measurements >140 mg/dl, 13% <80 mg/dl, and only 28% in the euglycemic range (80-140 mg/dl). After 4 weeks on pramlintide, measurements in the hyperglycemic range declined to 48% and measurements within the euglycemic range increased to 37%. This shift from the hyperglycemic to the euglycemic range occurred with a concomitant 17% reduction in mealtime insulin dosages and without relevant increases in measurements below the euglycemic range (15%) or any severe hypoglycemic events. After 4 weeks on pramlintide, postprandial glucose, glucagon, and triglyceride excursions were reduced by similar to 86, similar to 87, and similar to 72%, respectively (incremental areas under the curve, all P < 0.05 vs. baseline). At week 6 (off treatment), the 24-h glucose profile and postprandial glucose, glucagon, and triglyceride excursions approached pretreatment values. CONCLUSIONS - In this study, the addition of pramlintide to insulin therapy reduced excessive 24-h glucose fluctuations as well as postprandial glucose, glucagon, and triglyceride excursions in patients with type I diabetes intensively treated with insulin pumps.
引用
收藏
页码:1 / 8
页数:8
相关论文
共 26 条
[1]  
[Anonymous], 1995, DIABETES, V44, P968
[2]  
[Anonymous], 2002, CLIN DIABETES
[3]  
Bode B W, 2000, Diabetes Technol Ther, V2 Suppl 1, pS43
[4]   Limitations of conventional methods of self-monitoring of blood glucose - Lessons learned from 3 days of continuous glucose sensing in pediatric patients with type 1 diabetes [J].
Boland, E ;
Monsod, T ;
Delucia, M ;
Brandt, CA ;
Fernando, S ;
Tamborlane, WV .
DIABETES CARE, 2001, 24 (11) :1858-1862
[5]   FAILURE OF GLUCAGON SUPPRESSION CONTRIBUTES TO POSTPRANDIAL HYPERGLYCEMIA IN IDDM [J].
DINNEEN, S ;
ALZAID, A ;
TURK, D ;
RIZZA, R .
DIABETOLOGIA, 1995, 38 (03) :337-343
[6]  
Edelman Steven V, 2002, Diabetes Technol Ther, V4, P175, DOI 10.1089/15209150260007390
[7]   The human amylin analog, pramlintide, corrects postprandial hyperglucagonemia in patients with type I diabetes [J].
Fineman, MS ;
Koda, JE ;
Shen, LZ ;
Strobel, SA ;
Maggs, DG ;
Weyer, C ;
Kolterman, OG .
METABOLISM-CLINICAL AND EXPERIMENTAL, 2002, 51 (05) :636-641
[8]   Dose-response for glucagonostatic effect of amylin in rats [J].
Gedulin, BR ;
Rink, TJ ;
Young, AA .
METABOLISM-CLINICAL AND EXPERIMENTAL, 1997, 46 (01) :67-70
[9]  
Georgopoulos A, 1999, CLIN CARDIOL, V22, pII28
[10]  
Gottlieb A, 2000, DIABETES, V49, pA109