The Goto–Kakizaki (GK) rat offers a genetic model of type 2 diabetes and displays profoundly defective insulin secretion leading to basal hyperglycemia. This animal is widely used for studying type 2 diabetes. However, the morphological characteristics of the pancreatic islets of Langerhans in GK rats are not fully understood. The present study sought to clarify this issue using immunohistochemical and electron microscopic techniques. GK rats were killed at 7, 14, 21, and 35 weeks of age. Structural islet changes were not observed at 7 weeks old. At 14 and 21 weeks of age, GK rats displayed histopathological islet changes. The general shape of islets became irregular, and immunoreaction of β-cells against antiinsulin appeared diffusely weakened. Electron microscopy revealed that the numbers of so-called β-granules decreased and the numbers of immature granules increased. The Golgi apparatus of β-cells was developed and the cisternae of rough endoplasmic reticulum were often dilated, indicating hyperfunction of the cells. However, at 35 weeks old, immunoreactivities of dispersed β-cells into the exocrine portion recovered, and numbers of secretory granules increased again and features of the cell organelles did not display hyperfunction. These results suggest that insulin deficiency in GK rats is not caused by simple dysfunction and/or degeneration of β-cells but rather by more complicated events within cells.