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Growth hormone response to prostaglandin E2
Abstract:
C-AMP causes release of growth hormone from the pituitary. Prostaglandin increases pituitary adenylate cyclase and C-AMP and therefore acts like a growth hormone-releasing hormone. Using PGE2 (30 microgram per kilo body weight) given intravenously we have demonstrated that in no case was there a growth hormone response to insulin hypoglycaemia when PGE2 failed to evoke a response. However in 6 of 18 patients unresponsive to insulin hypoglycaemia a significant rise in growth hormone was obtained from PGE2. We argue that in these 6 patients hypothalamic unresponsiveness to hypoglycaemia must be operative whereas PGE2 acting directly at pituitary level is likely to have caused the release of preformed growth hormone from the pituitary. Administration of PGE2 does not cause hypoglycaemia but rather a slight rise in the plasma glucose level. Thus the risk of brain damage which is inherent in the insulin hypoglycaemia test is avoided.
Insights
Prostaglandin E2 (PGE2) can stimulate growth hormone release directly from the pituitary. This offers a safer alternative to insulin hypoglycemia testing for assessing growth hormone secretion.
Area of Science:
- Endocrinology
- Neuroendocrinology
Background:
- Cyclic adenosine monophosphate (C-AMP) mediates growth hormone (GH) release from the pituitary gland.
- Prostaglandin E2 (PGE2) increases pituitary adenylate cyclase and C-AMP, suggesting it functions as a growth hormone-releasing hormone.
Purpose of the Study:
- To evaluate the efficacy of PGE2 as a stimulus for GH release.
- To compare the GH response to PGE2 with the response to insulin-induced hypoglycemia.
- To assess the safety profile of PGE2 compared to insulin hypoglycemia testing.
Main Methods:
- Intravenous administration of PGE2 (30 µg/kg body weight) in patients.
- Assessment of growth hormone levels following PGE2 administration.
- Comparison with growth hormone response to insulin-induced hypoglycemia in the same patients.
Main Results:
- In patients unresponsive to insulin hypoglycemia, PGE2 elicited a significant GH rise in 6 out of 18 cases.
- When PGE2 failed to stimulate GH release, there was no GH response to insulin-induced hypoglycemia.
- PGE2 administration did not induce hypoglycemia; instead, it caused a slight increase in plasma glucose levels.
Conclusions:
- PGE2 acts directly on the pituitary to release preformed GH, bypassing potential hypothalamic dysfunction.
- PGE2 is a viable alternative to insulin hypoglycemia for assessing pituitary GH secretory capacity.
- PGE2 avoids the risk of hypoglycemia-associated brain damage inherent in the insulin tolerance test.