A low carbohydrate, high fiber diet containing a processed maize by-product increases the incidence and advances the onset of diabetes in NOD mice

Type I diabetes is reported to be caused by a combination of genetic predisposition, diet and immune exposure. Small animal models, such as the Non-obese diabetic (NOD) mouse, are often used to test potential therapies that may prevent, delay or cure the disease. This model of Type 1 diabetes may require large numbers of mice to demonstrate the effects of intervention to prevent or treat the disease and its sequelae. Our aim was to find a non-fat dietary component that would increase the incidence of Type 1 diabetes in the NOD mouse and allow smaller but statistically valid experiments. We have developed a relatively well-balanced diet that advances the mean age of onset of Type 1 diabetes from 209 days to 175 days and increases the incidence of Type 1 diabetes from approximately 50% to 76%. This diabetogenic diet was fed from weaning and contains a high proportion (58.5%) of a processed maize by-product high in fibre and protein but with low carbohydrate. Normal ground maize was not diabetogenic. Advanced glycosylation end-products, known to be toxic to pancreatic beta-cells, were measured and were higher in the diabetogenic processed maize diet than in the control diet. Our results suggest that this processed maize by-product, used principally as a farm animal feed throughout the developed world, promotes diabetes in the NOD mouse and is possibly caused by advanced glycosylation end-products.