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Drugs Not Linked to β-Cell Improvement in Diabetes

Last Updated: December 29, 2009.

The use of insulin, exenatide, and the immunosuppressant daclizumab doesn't lead to improved function of surviving β-cells in patients with long-standing type 1 diabetes, according to research published in the December issue of Diabetes Care.

TUESDAY, Dec. 29 (HealthDay News) -- The use of insulin, exenatide, and the immunosuppressant daclizumab doesn't lead to improved function of surviving β-cells in patients with long-standing type 1 diabetes, according to research published in the December issue of Diabetes Care.

Kristina I. Rother, M.D., of the National Institutes of Health in Bethesda, Md., and colleagues analyzed data from 16 adults with type 1 diabetes of an average duration of 21.3 years. After a period of intensified glucose control, subjects were randomized to receive insulin only, insulin plus exenatide to stimulate β-cell recovery, insulin plus daclizumab, or all three drugs.

The researchers found that all subjects had C-peptide levels of at least 0.3 ng/mL at baseline or following arginine stimulation, indicating endogenous insulin production. Arginine and mixed-meal stimulation of C-peptide decreased due to the intensified insulin treatment during the study run-in. Exenatide with or without daclizumab didn't significantly increase C-peptide secretion.

"In conclusion, residual β-cells may play an important role as a potential source of new β-cells in future trials, especially in younger patients and at an earlier stage of the disease. More combination therapies that include immunomodulators with agents that improve β-cell function and growth are needed to expand residual β-cell mass to a degree that individuals with type 1 diabetes may eventually become insulin independent," the authors write.

Amylin Pharmaceuticals provided partial funding for the study and is the employer of several co-authors.

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