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Single pancreatic beta-cells from normal rats exhibit an initial decrease and subsequent increase in cytosolic free

T Yada1, M Kakei, H Tanaka

  • 1Department of Physiology, Kagoshima University School of Medicine, Japan.

Cell Calcium
|January 1, 1992
PubMed
Summary

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Glucose stimulation causes a dual change in pancreatic islet cells

Area of Science:

  • Endocrinology
  • Cell Physiology
  • Metabolic Research

Background:

  • Controversy exists regarding the physiological relevance of initial glucose-induced cytosolic free calcium concentration ([Ca2+]i) decrease in pancreatic islet cells.
  • Previous studies in hyperglycemic mice suggested a biphasic [Ca2+]i response to glucose stimulation.

Purpose of the Study:

  • To investigate the physiological nature of the glucose-induced biphasic change in cytosolic free calcium concentration ([Ca2+]i) in pancreatic beta-cells.
  • To determine if the initial decrease and subsequent increase in [Ca2+]i are mediated by independent mechanisms.

Main Methods:

  • Measurement of cytosolic free calcium concentration ([Ca2+]i) in single pancreatic beta-cells from normal rats using Fura-2 microfluorometry.
  • Manipulation of basal and stimulatory glucose concentrations.

Related Experiment Videos

  • Experiments involving removal of extracellular calcium and use of mannoheptulose (a glucose metabolism inhibitor).

    • Main Results:

    • Elevating glucose from 2.8 mM to 16.7 mM induced a bimodal [Ca2+]i change (initial decrease, then increase) in normal rat beta-cells.
    • The initial [Ca2+]i decrease was observed even with lower glucose increments or in the absence of extracellular calcium, while the increase was calcium-dependent.
    • Mannoheptulose inhibited both the glucose-induced decrease and increase in [Ca2+]i, indicating dependence on glucose metabolism.

    Conclusions:

    • The glucose-induced biphasic change in cytosolic free calcium concentration ([Ca2+]i) is a physiological response in pancreatic islet beta-cells.
    • The initial decrease and subsequent increase in [Ca2+]i are regulated by distinct, mutually independent mechanisms dependent on glucose metabolism.