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Pancreatic beta cell replication induced by glucocorticoids in subhuman primates
The American Journal of Pathology
|May 1, 1974
Summary
Glucocorticoids increase pancreatic beta cell proliferation and insulin levels in monkeys. These effects are reversible, with beta cells surviving and maintaining function after treatment cessation.
Area of Science:
- Endocrinology
- Cell Biology
- Primate Research
Background:
- Adrenal glucocorticoids are known to affect glucose metabolism.
- The impact of glucocorticoids on pancreatic islet cell dynamics requires further elucidation.
Purpose of the Study:
- To investigate the effects of exogenous glucocorticoids on pancreatic islet morphology and function in Macaca cyclopis.
- To assess beta cell proliferation and insulin secretion in response to glucocorticoid administration.
Main Methods:
- Light microscopy, autoradiography, and electron microscopy were employed.
- Monkeys received glucocorticoid injections, and tissues were analyzed.
- (3)H-thymidine was used to label proliferating cells.
Main Results:
- Glucocorticoid treatment induced mild hyperglycemia and elevated serum insulin.
- Pancreatic beta cells showed degranulation and hyperplasia, with increased mitotic activity.
- These changes correlated with serum insulin levels and were reversible upon treatment cessation.
Conclusions:
- Glucocorticoids stimulate pancreatic beta cell proliferation and insulin production in primates.
- Newly formed beta cells are functional and survive after glucocorticoid withdrawal.
- No evidence of acinar-islet or duct-islet cell transformation was observed.