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Am J Physiol Endocrinol Metab (September 6, 2005). doi:10.1152/ajpendo.00216.2005
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Submitted on May 12, 2005
Accepted on August 31, 2005

Glucose-dependent increase in mitochondrial membrane potential, but not cytoplasmic calcium, correlates with insulin secretion in single islet cells

Emma Heart1, Richard F Corkey1, Jacob D Wikstrom2, Orian S Shirihai2, and Barbara E Corkey1*

1 Department of Medicine, Boston University School of Medicine, Boston, MA, USA
2 Department of Pharmacology, Tufts University School of Medicine, Boston, MA, USA

* To whom correspondence should be addressed. E-mail: bcorkey{at}bu.edu.

We examined the effects of different physiologic concentrations of glucose on cytoplasmic Ca2+ handling and mitochondrial membrane potential ({Delta} {Psi}m) and insulin secretion in single mouse islet cells. The threshold for both glucose-induced changes in Ca2+ and {Delta}{Psi}m ranged from 6 to 8 mM. Glucose step-jumps resulted in sinusoidal oscillations of cytoplasmic Ca2+, whereas {Delta}{Psi}m reached sustained plateaus with oscillations interposed on the top of these plateaus. The amplitude of the Ca2+ rise (height of the peak) did not vary with glucose concentration, suggesting a "digital" rather than "analog" character of this aspect of the oscillatory Ca2+ response. The average glucose-dependent elevation of cytoplasmic Ca2+ concentration during glucose stimulation reached saturation at 8 mM stimulatory glucose, whereas {Delta}{Psi}m showed a linear glucose dose-response relationship over the range of stimulatory glucose concentrations (4-16 mM). Glucose-dependent increases in insulin secretion correlated well with {Delta}{Psi}m, but not with average Ca2+ concentration. These data show that a K-ATP channel independent pathway is operative at the single cell level and suggest mitochondrial metabolism may be a determining factor in explaining graded, glucose dose-dependent increases in insulin secretion.




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