This study was undertaken to investigate
insulin-induced changes in the immunohistochemistry and morphometry of pancreatic beta-cells, plasma
insulin and
blood glucose concentrations of
streptozotocin (STZ)-treated diabetic rats. Fifty male Wistar rats (200-250 g) were randomly divided into three experimental groups (viz., A: control group, B: STZ-treated group, and C: STZ+insulin-treated group). Diabetes was induced in group B and group C rats by single
intraperitoneal injections of STZ (75 mg/kg
body weight), while each animal in the "control" group A received equal volume of
citrate buffer solution (pH 6.3) intraperitoneally. STZ+insulin-treated group C diabetic rats were additionally treated with
subcutaneous injections of
lente insulin (0.5 U/kg
body weight) daily from Day 10 to Day 30 of our 40-day study period. The rats used were sacrificed at different time intervals (10th, 20th, 30th and up to the 40th day) following STZ treatment. Fragments of endocrine pancreas of each rat were randomly processed for immunohistochemistry staining and pancreatic
insulin content. In diabetic state, pancreatic beta-cells showed a weak immunostaining for
insulin on Day 10. Thereafter,
insulin administration (in the group C rats) caused a significant decrease (p < 0.05) in the elevated
blood glucose levels, and a significant increase (p < 0.05) in the serum
insulin concentrations. The surviving beta-cells regenerated and virtually regained their normal immunostaining and functional status for
insulin. On the 30th day, the pancreatic
insulin contents of the
insulin-treated group C rats showed approximately 45-fold increase in immunoreactivity when compared with the immunoreactivity of the same STZ+insulin-treated rats on Day 10 of the 40-day study period. The present study illustrates the sequence of morphological changes that occur in the islets of Langerhans following STZ administration and subsequent
insulin treatment. The study also suggests that administration of a moderate single dose of STZ in Wistar rats produces specific
necrosis of beta-cells, typical of type 1
insulin-dependent diabetes. The experimental evidence obtained in this study appears to suggest that induction of regenerative stimulus (by
insulin treatment) in diabetic state triggers pancreatic regenerative processes, thereby restoring functional activities of the pancreas.