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J. Biol. Chem., Vol. 269, Issue 44, 27310-27314, 11, 1994
WF Pralong, A Spat and CB Wollheim
During cell activation, Ca2+, by stimulating the NADH-producing
mitochondrial dehydrogenases, triggers the generation of reducing
equivalents whereby ATP production is sustained. In cell populations,
[Ca2+] changes in the mitochondrial matrix were demonstrated to parallel
rapidly those in the cytosol ([Ca2+]i). There is still no indication as to
whether metabolic activation follows oscillatory patterns similar to those
of [Ca2+]i. Therefore, changes in NAD(P)H were monitored in single
pancreatic beta-cells, adrenal glomerulosa cells, and liver cells during
oscillatory [Ca2+]i transients. Rapid NAD(P)H and [Ca2+]i oscillations with
similar frequency and sensitive both to changes in glucose concentration
and to extracellular Ca2+ removal were identified in a subpopulation of
pancreatic beta-cells in primary culture. Furthermore, Ca(2+)-dependent
oscillatory NAD(P)H formation could be evoked by the pulsatile application
of depolarizing [K+], demonstrating the pacing effect of increased [Ca2+]i
on beta-cell metabolism. In adrenal glomerulosa cells, angiotensin II, a
physiological stimulator of aldosterone production, could be shown to
elicit the oscillatory formation of mitochondrial NAD(P)H through frequency
modulation of [Ca2+]i transients. In contrast to the two former endocrine
cell types, in hepatocytes, [Arg8]vasopressin and epinephrine caused the
amplitude modulation of NAD(P)H formation. Taken together, these results
provide unprecedented evidence for a cell- specific pacing of metabolism by
[Ca2+]i transients coordinated with cell activation and function.
Dynamic pacing of cell metabolism by intracellular Ca2+ transients
Department of Medicine, University of Geneva, Centre Medical Universitaire, Switzerland.
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