During the past two decades enough information has accumulated to classify Type-I diabetes (also termed insulin-dependent diabetes and for merly juvenile onset diabetes mellitus) as a chronic autoimmune disease. In this disorder, cells producing insulin ([3 cells) within the pancreatic islets are destroyed. These cells comprise the majority of islet cells but less than 2% of the total pancreatic mass (1, 2). Other endocrine islet cells such as those that synthesize the hormones glucagon or somatostatin are not destroyed in Type-I diabetes. With destruction of [3 cells and the resulting insulin deficiency, acute metabolic abnormalities develop which in the absence of insulin therapy lead to death in a state resembling accelerated starvation. Since 1922 and the advent of insulin therapy, the majority of acute deaths due to insulin deficiency have been prevented. Nevertheless patients with Type-I diabetes are at constant risk for severe hypoglycemia due to pharmacologic administration of insulin, and the majority develop a series of morbid and often mortal complications including renal failure, proliferative retinopathy leading to blindness, and neuropathic syndromes. There is extensive circumstantial evidence that the incidence and severity of diabetic secondary complications correlate with the degree of metabolic control. This circumstantial evidence has been strengthened during the past decade with the availability of the means to monitor average blood