Indexed on: 01 Jun '70Published on: 01 Jun '70Published in: Diabetologia
Electronmicroscopic studies were performed on the pancreatic islets of normal mice (C 57BL/ KsJ) and of diabetic mutants (C 57 BL/Ks-db/db) at all stages of the syndrome. The ultrastructural appearance of the islets of prehyperglycemic mutants (Blood Glucose < 120 mg/100 ml) did not differ from that of normal mice. The two could not be differentiated without the aid of radioautography, which demonstrated that the beta cells of prehyperglycemic mutants incorporated thymidine-3H with greater frequency. Beta cells of early hyperglycemic mice (BG 130–200 mg/100 ml) revealed partial secretory degranulation, increased quantities of rough endoplasmic reticulum and enlarged Golgi structures. Beta cell necrosis was most common in mice with established hyperglycemia during the period of most rapid blood glucose elevation. It negated the effects of the short lived increase in beta cell proliferation and was eventually responsible for a reduction in beta cell mass and relative insulin insufficiency. The presence of unique intra-islet ductal structures and acinar cells later in the syndrome is unknown in other diabetic models. The proliferating ductal epithelial cells presumably gave rise to ciliated cells, mucous goblet or Paneth cells and pancreatic acinar cells, but no evidence of beta cell neogenesis was obtained. “Virus-like” particles were identified within intact and necrotic beta cells and intra-islet acinar cells.