Amylin is a proteinaceous hormone secreted form insulin-producing pancreatic beta-cells following stimulation by food molecules such as glucose and arginine. Amylin decreases insulin-stimulated glucose uptake in skeletal muscle and counteracts the ability of insulin to suppress output of glucose from the liver. Substantial evidence supports the view that maylin is a second glucoregulatory hormone produced from islet beta-cells, which can modulate a number of metabolic processes also regulated by insulin. The islet beta-cell may therefore transmit a dual message to peripheral tissues through the two hormones, insulin and amylin. Like insulin, amylin is deficient in individuals with autoimmune diabetes mellitus. Since amylin can modulate processes of fuel metabolism in key tissues, amylin deficiency could contribute to the clinical course in patients with autoimmune diabetes. Here, I propose that amylin lack plays a significant role to promote the tendency to hypoglycemia and defective glycemic control characteristic of insulin-treated patients with autoimmune diabetes. Treatment of such diabetics with injections of amylin as well as insulin is being evaluated with the aim of lessening the incidence and severity of hypoglycemia and improving glycemic control.