EurekaMag.com logo
+ Site Statistics
References:
52,725,316
Abstracts:
28,411,598
+ Search Articles
+ Subscribe to Site Feeds
EurekaMag Most Shared ContentMost Shared
EurekaMag PDF Full Text ContentPDF Full Text
+ PDF Full Text
Request PDF Full TextRequest PDF Full Text
+ Follow Us
Follow on FacebookFollow on Facebook
Follow on TwitterFollow on Twitter
Follow on Google+Follow on Google+
Follow on LinkedInFollow on LinkedIn

+ Translate

Regulation of hepatic glycogen synthesis during fetal development: roles of hydrocortisone, insulin, and insulin receptors


Proceedings of the National Academy of Sciences of the United States of America 70(12): 3454-3457
Regulation of hepatic glycogen synthesis during fetal development: roles of hydrocortisone, insulin, and insulin receptors
In fetal rat liver in utero, an increase in glycogen and the glycogen synthetic enzyme glycogen synthetase (EC 2.4.1.11) occurs between gestational days 17 and 19. We used an organ culture system for finding the stimulus for increased enzyme activity and defining the relationship of this increase to glycogen synthesis. In fetal-liver explants from an earlier period (gestational day 16), hydrocortisone causes an elevation in total glycogen synthetase activity. This effect, which can be blocked by actinomycin D, is strikingly similar in time course and magnitude to the normal increase in utero. However, in order for glycogen synthesis to proceed after hydrocortisone increases glycogen synthetase levels, insulin is required. Unlike hydrocortisone, insulin does not increase total glycogen synthetase; it appears to act by converting the b or phospho form of synthetase to the a or dephospho form. Insulin alone does not stimulate glycogen synthesis in explants from 16-day fetal liver, although no defect in insulin binding was demonstrable. These findings support the hypothesis that the increase in liver-glycogen synthesis during the last trimester requires glucocorticoids for the developmental induction of glycogen synthetase and insulin for activation of the enzyme.


Accession: 006288402

PMID: 4357871

DOI: 10.1073/pnas.70.12.3454



Related references

Insulin-like growth factor 2 and the insulin receptor, but not insulin, regulate fetal hepatic glycogen synthesis. Endocrinology 151(2): 741-747, 2010

The roles of insulin and glucagon in the regulation of hepatic glycogen synthesis and turnover in humans. Journal of Clinical Investigation 97(3): 642-648, 1996

Regulation of hepatic glycogen synthetase of rana catesbeiana effect of insulin and hydrocortisone on glycogen synthetase in a liver system in vitro and regulation of glycogen synthetase by cellular metabolites. Journal of Biological Chemistry 246(4): 873-880, 1971

Developmental regulation of fetal rat liver glycogen synthetase by hydrocortisone and insulin. Federation Proceedings 32(3 PART 1): 253, 1973

The role of insulin and glucagon in the regulation of hepatic glycogen synthesis and turnover in humans. Journal of Clinical Investigation 97(3): 642-648, 1996

Time-dependent regulation of insulin receptors, GLUT4, hexokinase II, and glycogen synthase by insulin in rat muscles. Diabetologia 40(SUPPL 1): A282, 1997

Effect of down-regulation and return of insulin receptors on glycogen synthesis in cultured rat hepatocytes. Biochimica et Biophysica Acta 888(2): 191-198, 1986

Characterization of insulin-like actions of anti-insulin receptor antibodies. Effects on insulin binding, insulin degradation, and glycogen synthesis in isolated rat hepatocytes. Journal of Biological Chemistry 255(9): 4028-4034, 1980

Dependence on insulin of the apparent hydrocortisone activation of hepatic glycogen synthetase. Proceedings of the National Academy of Sciences of the United States of America 58(4): 1515-1519, 1967

Insulin and the stimulation of glycogen synthesis. The road from glycogen structure to glycogen synthase to cyclic AMP-dependent protein kinase to insulin mediators. Advances in Enzymology and Related Areas of Molecular Biology 63: 173-231, 1990