Recent data suggest that in a proportion of NIDDM patients there is a slowly evolving insulitis which results in a latent autoimmune diabetes leading to full insulin-dependence. Many animal models exist of NIDDM but none have reported the spontaneous existence of a similar phenomenon. We have re-examined the histology of pancreata from a few Psammomys obesus who had become insulin-dependent in the late stages of NIDDM. We report here the unexpected finding of the presence of insulitis in these animals and suggest that they could be a model for the clinical observation of latent IDDM in NIDDM patients.
A morphological analysis of the endocrine pancreas in the normoglycemic sand rat (Psammomys obesus) has been carried out and the immunoreactivity for insulin, glucagon, somatostatin and pancreatic polypeptide (PP) studied. The islets of both parts of the pancreas (pancreatic head and tail) investigated were of the 'mantle' type: centrally located B-cells and A-, D- and PP-cells at the periphery. In the 'glucagon islets' (tail of pancreas) predominated the A-cells, while the PP-cells were more abundant in the "PP-islets' (head of the pancreas).
The abdominal cavity of male albino rats, average weight 250 g, was opened and the duodenum approached where the ductus choledochus joins. Pancreatic ducts empty into the lower third of the choledochus. The ductus choledochus was cannulated with a Teflon catheter beneath the liver and its other end was brought out at the neck of the rat. Tissue glue was introduced into the lower part of the choledochus towards the liver. Another Teflon catheter was introduced into the duodenum, its second end brought out at the neck and connected with the first catheter by means of a metal tube, thus preserving bile flow from the liver to the duodenum. Tissue glue injection resulted in complete atrophy of the exocrine pancreas within 2–15 days. The islets of Langerhans remained intact.
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