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Thapsigargin inhibits the glucose-induced decrease of intracellular Ca2+ in mouse islets of Langerhans

M W Roe1, R J Mertz, M E Lancaster

  • 1Department of Cell Physiology, Glaxo Research Institute, Research Triangle Park, North Carolina 27709.

The American Journal of Physiology
|June 11, 1994
PubMed
Summary

Glucose initially lowers intracellular calcium in pancreatic islets, a process called phase 0. This effect is linked to enhanced beta-cell SERCA activity, crucial for glucose metabolism and insulin secretion.

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Area of Science:

  • Endocrinology
  • Cell Biology
  • Metabolic Research

Background:

  • Pancreatic islets of Langerhans regulate blood glucose via insulin secretion.
  • Glucose stimulation is known to alter intracellular calcium concentration ([Ca2+]i) in beta-cells.

Purpose of the Study:

  • To investigate the earliest changes in intracellular calcium concentration ([Ca2+]i) following glucose stimulation in pancreatic islets.
  • To elucidate the mechanisms underlying the initial glucose-induced alteration of [Ca2+]i.

Main Methods:

  • Mouse pancreatic islets were loaded with fura 2 to measure intracellular calcium.
  • Extracellular glucose concentrations were varied (e.g., 2 to 12 mM, 5 to 12 mM).
  • The effects of various substances (D-glyceraldehyde, 2-deoxyglucose, glyburide, mannoheptulose, thapsigargin) on [Ca2+]i were assessed.

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Main Results:

  • The earliest glucose-induced change in [Ca2+]i was a rapid and pronounced decline (phase 0).
  • Phase 0 was observed consistently and was mimicked by D-glyceraldehyde but not other agents.
  • Inhibition of sarcoplasmic/endoplasmic reticulum Ca2+-ATPase (SERCA) by thapsigargin abolished the glucose-induced [Ca2+]i reduction.

Conclusions:

  • Glucose stimulation of pancreatic islets initially causes a decrease in intracellular calcium ([Ca2+]i).
  • This effect is mediated by an increase in beta-cell SERCA activity, likely triggered by glycolytic intermediates.