DIETARY COWS MILK PROTEIN DOES NOT ALTER THE FREQUENCY OF DIABETES INTHE BB RAT

One theory of the pathogenesis of IDDM proposes that exposure to cow's milk proteins triggers the disease in genetically susceptible individ uals. We tested this hypothesis in the BB/Wor rat model of human IDDM. Diabetes-prone (DP) BB/Wor rats spontaneously develop IDDM. Coisogeni c diabetes-resistant (DR) BB/Wor rats do not develop diabetes spontane ously, but IDDM can readily be induced by treatment with polyinosinic: polycytidylic acid and depletion of BT6(+) T-cells. Pregnant BB/Wor ra ts were fed one of four experimental diets or a standard Purina commer cial rat chow (5010) that was certified to be free of cow's milk prote in. Offspring were maintained on the maternal diet after weaning. DP-B B/Wor rats, fed either of two experimental diets based on hydrolyzed c asein and free of intact milk protein (Nutramigen or D11236), develope d diabetes at only half the rate of animals fed Purina 5010 chow. Neit her the addition of bovine serum albumin (BSA) to Nutramigen nor the s ubstitution of total milk protein for the hydrolyzed casein in the D11 236 diet increased the frequency of spontaneous diabetes. In contrast, there was no relationship between diet and susceptibility of DR-BB/Wo r rats to IDDM induction. However, the methods used to induce IDDM in DRBB/Wor animals were found to induce antibodies against BSA. We concl ude the following: 1) Dietary modification can reduce spontaneous IDDM expression in DP-BB/Wor rats, but the agent of protection is not elim ination of cow's milk protein. 2) The addition of BSA or intact milk p rotein does not abrogate the effectiveness of a protective diet. 3) Th e genetic susceptibility of the DR-BB/Wor rat to autoimmune diabetes i s unaffected by any of the tested diets, but a role of anti BSA-like a utoreactivity in IDDM expression cannot be excluded.