Glucose Metabolism Regulates Cytosolic Ca2+ in the Pancreatic β-Cell by Three Different Mechanisms

  • Angel Nadal
  • Bernat Soria
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 426)


The main stimulus to promote insulin release is an increase in the extracellular glucose concentration. It has been repeatedly shown that glucose and other secretagogues induced an increase in cytosolic Ca2+ ([Ca2+]i). The sequence of events linking exposure to stimulatory glucose concentrations with the release of insulin has been established [1]. Glucose-induced [Ca2+]i increase is a consequence of glucose metabolism, ATP generation and blockade of ATP-dependent K+ channels [2,3] which in turn depolarize the cell and activate voltage-dependent Ca2+ channels [4]. According to this mechanism it was demonstrated that glucose-induced [Ca2+]i oscillations [5] are due to bursting of the electrical activity [6]. Moreover, simultaneous measurement of KATP channel activity and [Ca2+]i in isolated β-cells showed that blockade of KATP always precedes [Ca2+]i increase and that there is a strict correlation between spike frequency and Ca2+ increase [7]. All this body of theory was in apparent contradiction with other results which indicate that under certain conditions glucose decreased [Ca2+]i [8]. It should be noted that the physiological effect of glucose on [Ca2+]i is neither a decrease nor a steady-state increase in [Ca2+]i but the induction of well-shaped [Ca2+]i oscillations in islet cells. A detailed description of such oscillations is given in Chapter 26.


Glucose Metabolism Pancreatic Islet Fluorescence Quenching Total Fluorescence Muscarinic Agonist 
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Copyright information

© Springer Science+Business Media New York 1997

Authors and Affiliations

  • Angel Nadal
    • 1
  • Bernat Soria
    • 1
  1. 1.Center for Bioengineering, Department of PhysiologyMiguel Hernandez UniversityAlicanteSpain

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