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Am J Physiol Endocrinol Metab 290: E143-E148, 2006. First published September 6, 2005; doi:10.1152/ajpendo.00216.2005
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Glucose-dependent increase in mitochondrial membrane potential, but not cytoplasmic calcium, correlates with insulin secretion in single islet cells

Emma Heart,1 Richard F. Corkey,1 Jacob D. Wikstrom,2 Orian S. Shirihai,2 and Barbara E. Corkey1

1Department of Medicine, Obesity Research Center, Boston University School of Medicine and 2Department of Pharmacology and Experimental Therapeutics, Tufts University School of Medicine, Boston, Massachusetts

Submitted 12 May 2005 ; accepted in final form 31 August 2005

We examined the effects of different physiological 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 an ATP-dependent K+ channel-independent pathway is operative at the single cell level and suggest mitochondrial metabolism may be a determining factor in explaining graded, glucose concentration-dependent increases in insulin secretion.


Address for reprint requests and other correspondence: B. E. Corkey, Obesity Research Center, Boston Univ. School of Medicine, 650 Albany St., EBRC 840, Boston, MA 02118 (e-mail: bcorkey{at}bu.edu)




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