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Am J Physiol Cell Physiol 274: C1174-C1184, 1998;
0363-6143/98 $5.00
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Vol. 274, Issue 4, C1174-C1184, April 1998

MODELING IN PHYSIOLOGY
Model of beta -cell mitochondrial calcium handling and electrical activity. II. Mitochondrial variables

Gerhard Magnus1 and Joel Keizer1,2

1 Institute of Theoretical Dynamics and 2 Section on Neurobiology, Physiology, and Behavior, University of California, Davis, California 95616

In the preceding article [Am. J. Physiol. 274 (Cell Physiol. 43): C1158-C1173, 1998], we describe the development of a kinetic model for the interaction of mitochondrial Ca2+ handling and electrical activity in the pancreatic beta -cell. Here we describe further results of those simulations, focusing on mitochondrial variables, the rate of respiration, and fluxes of metabolic intermediates as a function of D-glucose concentration. Our simulations predict relatively smooth increases of O2 consumption, adenine nucleotide transport, oxidative phosphorylation, and ATP production by the tricarboxylic acid cycle as D-glucose concentrations are increased from basal to 20 mM. On the other hand, we find that the active fraction of pyruvate dehydrogenase saturates, due to increases in matrix Ca2+, near the onset of bursting electrical activity and that the NADH/NAD+ ratio in the mitochondria increases by roughly an order of magnitude as glucose concentrations are increased. The mitochondrial ATP/ADP ratio increases by factor of <2 between the D-glucose threshold for bursting and continuous spiking. According to our simulations, relatively small changes in mitochondrial membrane potential (~1 mV) caused by uptake of Ca2+ are sufficient to alter the cytoplasmic ATP/ADP ratio and influence ATP-sensitive K+ channels in the plasma membrane. In the simulations, these cyclic changes in the mitochondrial membrane potential are due to synchronization of futile cycle of Ca2+ from the cytoplasm through mitochondria via Ca2+ uniporters and Na+/Ca2+ exchange. Our simulations predict steady mitochondrial Ca2+ concentrations on the order of 0.1 µM at low glucose concentrations that become oscillatory with an amplitude on the order of 0.5 µM during bursting. Abrupt increases in mitochondrial Ca2+ concentration >5 µM may occur during continuous electrical activity.

pancreatic beta -cell; kinetic model


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