The ultrastructural distribution of β cell ballooning degeneration was studied in 50 per cent depancreatized dogs which were rendered severely diabetic by daily growth hormone administration varying from ten to twenty-eight days. At ten days most β cells showed infiltration by glycogen granules, distortion of mitochondria, prominence of Golgi complex and presence of small, empty, membrane-bound vacuoles. The vacuoles increased in size and number parallel with the duration of the diabetic state. After twenty-one days of treatment many β cells were riddled with numerous membrane-bound vacuoles frequently separated by thin septa. The intervening cytoplasm still showed presence of glycogen. There was extensive β cell de granulation noticeable, although some cells still contained a few residual or newly formed granules indicating active insulinogenesis. At four weeks of treatment the septa separating the vacuoles were frequently broken so that several vesicles merged to form larger spaces. The α cells were intact, except for two animals in which they contained glycogen. The δ cells were not definitely identified. The ductal epithelium was intact. However, the cytoplasm frequently contained glycogen and small, membrane-bound granules.

It is hypothesized that the vacuoles originate most likely from distended vesicular ergastoplasm although the possibility that they arise from distended Golgi vesicles or vacuolated mitochondria cannot be ruled out. The present study suggests that vacuolization of β cells is the ultramicroscopic equivalent of the ballooning degeneration previously observed by light microscopy. They also confirm the previously established hypothesis that β cell glycogenization is a lesion independent from ballooning degeneration.

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