Journal article
The effect of acetylglyceryl ether phosphorylcholine on glycogenolysis and phosphatidylinositol 4,5-bisphosphate metabolism in rat hepatocytes
The Journal of biological chemistry, Vol.259(14), pp.8685-8688
07/25/1984
DOI: 10.1016/S0021-9258(17)47205-X
PMID: 6086606
Abstract
The effect of acetylglyceryl ether phosphorylcholine (AGEPC) on glycogenolysis and phosphatidylinositol 4,5-bisphosphate has been studied in rat hepatocytes. Previously, this laboratory demonstrated that AGEPC stimulated glucose output from the perfused rat liver and promoted the breakdown of phosphoinositides in rat hepatocytes (Shukla, S. D., Buxton, D. B., Olson, M.S., and Hanahan, D.J. (1983) J. Biol. Chem. 258, 10212-10214). In the present study, addition of AGEPC (10(-13) to 10(-9) M) to rat hepatocytes failed to stimulate glucose output, whereas epinephrine (10(-5)M) and glucagon (10(-7)M) stimulated glucose output by 100% or more in these same cells. The effects of AGEPC, epinephrine, vasopressin, and glucagon on glycogen phosphorylase activity and the breakdown of phosphatidylinositol 4,5-bisphosphate were compared in hepatocytes. AGEPC (10(-9)M) promoted the breakdown of phosphatidylinositol 4,5-bisphosphate in a fashion similar to epinephrine (10(-5)M) and vasopressin (10(-7)M). In contrast to the two calcium-mobilizing hormones, epinephrine and vasopressin, AGEPC did not cause an activation of glycogen phosphorylase. Glucagon activation of glycogen phosphorylase was not accompanied by a significant effect on phosphatidylinositol 4,5-bisphosphate hydrolysis. Thus, AGEPC is a chemical mediator which induces the degradation of phosphatidylinositol 4,5-bisphosphate without activating glycogenolysis in hepatocytes.
Details
- Title: Subtitle
- The effect of acetylglyceryl ether phosphorylcholine on glycogenolysis and phosphatidylinositol 4,5-bisphosphate metabolism in rat hepatocytes
- Creators
- Rory A FisherShivendra D ShuklaMichael S DebuysereDonald J HanahanMerle S Olson
- Resource Type
- Journal article
- Publication Details
- The Journal of biological chemistry, Vol.259(14), pp.8685-8688
- DOI
- 10.1016/S0021-9258(17)47205-X
- PMID
- 6086606
- NLM abbreviation
- J Biol Chem
- ISSN
- 0021-9258
- eISSN
- 1083-351X
- Publisher
- United States
- Grant note
- AM-33538 / NIADDK NIH HHS
- Language
- English
- Date published
- 07/25/1984
- Academic Unit
- Iowa Neuroscience Institute; Neuroscience and Pharmacology; Internal Medicine
- Record Identifier
- 9984040249502771
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