Theoretical Chronobiology Unit
Free University of Brussels CP231
B-1050 Brussels, Belgium
Joint work with Erika Baus and Albert Goldbeter.
In many cell types, Ca2+ controls specific cellular processes such as contraction, secretion and metabolic pathways. The Ca2+ rise induced by external stimulation often consists of a series of transients, whose frequency increases with the dose of agonist (Berridge, 1997). In the liver, such Ca2+oscillations can be induced by the hormones vasopressin and phenylephrine as well as by the neurotransmitter noradrenaline (Woods et al., 1986). These three agonists moreover lead to the release of glucose from glycogen in hepatocytes. This effect is known to be mediated by the stimulation of phosphorylase kinase activity by the Ca2+/calmodulin complex. The latter kinase indeed induces the transformation of the glycogen phosphorylase into an active form, which degrades glycogen into glucose. By extending a model previously developped to study the switch between glycogen synthesis and degradation in the liver (Cardenas and Goldbeter, 1996), we analyze theoretically the effect of Ca2+ oscillations on the fraction of active phosphorylase kinase. We predict that Ca2+ oscillations can potentiate glycogen degradation at low stimulation levels.
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