The difference in the glycemic response to a high-fat diet between SDT and ZDF rats might be explained by a vulnerability of the pancreatic beta cells to lipid accumulation initiated by high-fat intake in the latter, whereas the SDT rat is more vulnerable to glucose loading that increases insulin demand and leads to beta cell failure and hypoinsulinemia, all of which emphasizes the role of diet composition in diabetes outcomes in these models. This evidence concerns the gene INS and diabetes mellitus.