Abstract
One of the hallmarks of endotoxemia is the impairment of glucose homeostasis (Hinshaw, 1976). The liver is a major site of glycogen storage and plays a pivotal role in the homeostasis of blood glucose. Glycogen synthesis and breakdown, and gluconeogenesis are under strict hormonal regulation. Besides the well known stimulators of glycogenolysis, i.e. glucagon, epinephrine, vasopressin (VP) (Kraus-Friedman 1984; Exton 1985), other factors e.g. the tumor-promoter phorbol ester, phorbol 12-myristate 13-acetate (PMA) (Garcia-Sainz and Hernandez-Sotomayor 1985) and platelet-activating factor (PAF) (Shukia et al 1983) also stimulate hepatic glycogenolysis. Endotoxemia is also associated with alterations in hepatic fatty acid and oxidation and ketogenesis (Wannemacher et al 1981).
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Spitzer, J.A. (1991). Modulation of Hepatic Function in Endotoxemia by Intercellular Communication. In: Schlag, G., Redl, H., Siegel, J.H., Traber, D.L. (eds) Shock, Sepsis, and Organ Failure. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-76511-7_10
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DOI: https://doi.org/10.1007/978-3-642-76511-7_10
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