Since insulin was first administered on January 11, 1922 (1), treatment of patients with type 1 diabetes has attempted to restore the metabolic abnormalities associated with autoimmune P-cell destruction and insulin deficiency. The ensuing decades have seen many advances in our understanding of insulin physiology, pharmacokinetics, and therapeutics, and the resultant development of purified insulin, recombinant human insulin, and insulin analogs. However, complete metabolic normalization with exogenous insulin therapy in such patients remains infrequent. The Diabetes Control and Complications Trial (DCCT) established conclusively that this inadequate metabolic control results in the long-term microvascular complications of diabetes (2). To minimize these complications, insulin-treatment regimens must mimic the complex secretion of insulin by the P-cells of the healthy pancreas. This task, however, remains a challenging goal (3).
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