Pancreatic islet ultrastructure, serum and pancreatic immunoreactive insulin in somatotrophic and metasomatotrophic diabetes in dogs.

Pancreatic ultrastructure as well as serum and pancreatic immunoreactive insulin content have been studied in nonoperated dogs rendered diabetic by the administration of growth hormone. In somatotrophic diabetes, the beta cells of the Langerhans islets were markedly degranulated and showed dilatation and prominence of the Golgi apparatus, cytoplasmic storage of glycogen, abnormalities of mitochondria as well as dilatation, vesiculation, degranulation and disruption of the endoplasmic reticulum. In some beta cells, damage was very severe and advanced. Accumulation of fat droplets and glycogen granules was found in the ductular epithelium. Fat droplets were also seen in the cytoplasm of a few alpha and acinar cells, however, these cells and the delta cells exhibited no major changes. In dogs with metasomatotrophic diabetes, neither regranulation nor neogenesis of beta cells were noted. Cytoplasmic glycogen storage was still apparent in both the beta and ductular epithelium cells. The serum insulin level was elevated in somatotrophic diabetes and reduced in metasomatotrophic diabetes; whereas, pancreatic immunoreactive insulin was decreased in somatotrophic diabetes and, to a greater extent, in metasomatotrophic diabetes. Present findings are consistent with the hypothesis that metasomatotrophic diabetes is a consequence of the overactivity, exhaustion and atrophy of the beta cells of the pancreatic islets produced by growth hormone.