A New Way to Reduce Both Postprandial Glucose and Oxidative Stress!
Abstract & Commentary
With Comment by Ralph R. Hall, MD, FACP, Emeritus Professor of Medicine University of Missouri- Kansas City School of Medicine and Associate Editor, Internal Medicine Alert.
Synopsis: Pramlintide reduces postprandial glucose excursions and oxidative stress in type 1 diabetes when given with short acting insulin at mealtime.
Source: Ceriello A, et al. Diabetes Care. 2005;28:632-637.
Oxidative stress has been shown to be increased in the postprandial period in patients with diabetes and has been implicated in the pathogenesis of micro- and macrovascular complications.
In order to measure the effects of pramlintide on oxidative stress and postprandial glucose Ceriello and associates designed a randomized, single-blind, controlled, crossover study. Nineteen subjects with type 1 diabetes underwent 2 standardized breakfast meal tests and received pramlintide or placebo in addition to their preprandial insulin. The plasma concentrations of glucose and markers of oxidative stress (nitrotyrosine, oxidized LDL [ox-LDL]), and total radical trapping antioxidant parameter (TRAP) were measured at baseline and during the 4 hour postprandial period.
Compared with placebo, pramlintide treatment significantly reduced postprandial glucose excursions, nitrotyrosine, ox-LDL, and prevented decline in TRAP.
Correlation analysis, adjusted for treatment revealed a significant association between postprandial mean incremental area under the curve (AUC) from 0 to 4 hours (AUC, 0-4 h) for glucose and postprandial mean incremental (AUC 0-4 h) for each measure of oxidative stress and TRAP (P < 0.001 for all correlations).
These findings indicate that the postprandial lowering effect of pramlintide in type 1 diabetes is associated with a significant reduction in postprandial oxidative stress.
Comment
This is a drug that you need to know more about! On March 16th 2005, Pramlintide (SYMLIN®), was approved by the Food and Drug Administration for use in conjunction with insulin. It is to be used at mealtime in patients with type 1 diabetes who have failed to achieve desired glucose control, despite optimal insulin therapy. It also may be used in type 2 diabetes, and in patients who are receiving mealtime insulin. Additional prescribing information can be obtained at www.SYMLIN.com.
Previous studies have suggested that postprandial glucose is a stronger predictor of cardiovascular disease than fasting glucose.1 Treatment with pramlintide may then be associated not only with better glucose control but also with better long-term survival and morbidity.
Pramlintide is a stable, injectable, synthetic, analog of amylin which was discovered to be secreted with insulin in 1987.2,3 It is a neuroendocrine hormone that restrains vagus-mediated gastric emptying and thereby slows carbohydrate absorption. It also suppresses hepatic glucose output. In animal studies it was found to induce post-prandial satiety and weight loss. This is a potential benefit because of the associated weight gain in patients receiving insulin.3
The physiology of amylin is a hot topic not only in diabetes but also in the prevention of Alzheimer’s disease. You will be hearing a great deal more about amylin in the future. Hull’s et al review3 is an excellent source of the current information regarding the pathophysiology of amylin secretion and accumulation in islet cells as well as in the central nervous system.
Note: The blinded parties in this study are the investigators performing the tests and the statistical evaluation.
References
1. Ceriello A, et al. Diabetologia. 2003;46 (Suppl 1): M9-M16.
2. Kieppinger EL, Vivian EM. Ann Pharmacother. 2003; 37:1082-1089.
3. Hull RL, et al. J Clin Endocrinol Metab. 2004;89: 3629-3643.
Pramlintide reduces postprandial glucose excursions and oxidative stress in type 1 diabetes when given with short acting insulin at mealtime.
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