Oral insulin both delays and reduces the frequency of autoimmune insulin-dependent diabetes mellitus (IDDM) in the NOD mouse,'possibly by generating populations of suppressor T cells. 2 The effects of this treatment in the BB rat are unknown. Diabetesprone (DP) BB rats spontaneously develop pancreatic insulitis followed by selective destruction of beta cells and diabetes between 50-90 days of age. 3 DP-BB rats are severely lymphopenic. Diabetes-resistant (DR) BB rats are coisogenic, nonlymphopenic descendants of DP-BB forebears. Their cumulative incidence of spontaneous diabetes is 4%. but they retain susceptibility to IDDM ind~ ction.~ They become diabetic if depleted of RT6'T cells and/or treated with the interferon inducer, polyinosinic: polycytidylic acid (poly I: C). 4 Like the NOD mouse, the BB rat is used to model human IDDM. We tested the hypothesis that oral insulin would prevent IDDM in the BB rat.