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Glucocorticoids and hepatic glycogen metabolism
Monographs on Endocrinology
|January 1, 1979
Summary
Glucocorticoids promote glycogen deposition in fetal and adult rat livers by inducing key enzymes like glycogen synthase. Insulin further enhances this process in fetal livers after glucocorticoid exposure.
Area of Science:
- Biochemistry
- Endocrinology
- Developmental Biology
Background:
- Glucocorticoids are crucial for fetal liver development.
- Glycogen synthesis is vital for energy storage in the liver.
Purpose of the Study:
- To investigate the role of glucocorticoids and insulin in fetal and adult rat liver glycogen deposition.
- To elucidate the enzymatic mechanisms underlying glucocorticoid-induced glycogenesis.
Main Methods:
- Administration of glucocorticoids and insulin to fetal and adult rats.
- Enzyme activity assays for glycogen synthase and phosphorylase.
- Analysis of enzyme interconversion systems.
Main Results:
- Glucocorticoids induce glycogen synthase and activate glycogen synthase phosphatase in fetal and adult rat livers.
- Insulin enhances glycogen deposition in glucocorticoid-primed fetal livers.
- Glucocorticoids inactivate glycogen phosphorylase in adult livers via phosphatase activation and a novel protein factor.
Conclusions:
- Glucocorticoids are primary regulators of liver glycogen accumulation during development and in adulthood.
- Enzyme activation, particularly of glycogen synthase phosphatase, is key to glucocorticoid action.
- Insulin acts synergistically with glucocorticoids in fetal liver glycogenesis.