Abstract
Many studies have indicated that the regulatory effects of hormones on glycogenolysis in the rat liver occur by at least two distinct mechanisms. While glucagon andß-adrenergic agonists stimulate hepatic glycogenolysis via cAMP-dependent protein kinase activation,α-adrenergic hormones as well as vasopressin and angiotension II mediate their effects by mechanisms independent of cAMP (Hems and Whitton, 1980; Extonet al., 1981). Con vincing experimental evidence suggests that alterations in cellular calcium fluxes leading to increases in the cytosolic calcium concentration and subsequent activation of phosphorylase kinase are involved in the glycogenolytic actions of the cAMP-independent hormones (Blackmoreet al., 1978; Murphyet al., 1980). Studies in several laboratories have indicated a possible second-messenger role of inositol-1,4,5-trisphosphate, a breakdown product of phosphatidylinositol-4,5-bisophosphate, in the calcium-mobilizing properties of these hormones (Berridge, 1984; Williamsonet al., 1985). The glycogenolytic actions of both glucagon and calcium-mobilizing hormones are observed in isolated hepatocytes, which constitute approximately 90% of the liver volume and are the primary site of glycogen storage in the liver.
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© 1989 Plenum Press, New York
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Fisher, R.A., Steinhelper, M.E., Olson, M.S. (1989). Regulatory Effects of a Thromboxane A2Analogue on Hepatic Glycogenolysis and Vasoconstriction. In: Fiskum, G. (eds) Cell Calcium Metabolism. GWUMC Department of Biochemistry Annual Spring Symposia. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5598-4_39
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DOI: https://doi.org/10.1007/978-1-4684-5598-4_39
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