Cadmium-induced insulin release does not involve changes in intracellular handling of calcium

Thomas Nilsson, Per Olof Berggren, Bo Hellman

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15 Scopus citations


A possible interaction between Cd2+ and Ca2+ as a component in Cd2+-induced insulin release was investigated in β cells isolated from obese hyperglycemic mice. The glucose stimulated Cd2+ uptake was dependent on the concentration of sugar. This uptake was sigmoidal with a Km for glucose of about 5 mM and was suppressed by both 50 μM of the voltage-activated Ca2+ channel blocker D-600 and 12 mM Mg2+. In the presence of 8 mM glucose 5 μM Cd2+ evoked a prompt and sustained stimulatory response, corresponding to about 3-fold of the insulin release obtained in the absence of the ion. Whereas 5 μM Cd2+ was without effect on the glucose-stimulated 45Ca efflux in the presence of extracellular Ca2+, 40 μM inhibited it. At a concentration of 5 μM, Cd2+ had no effect on the resting membrane potential or the depolarization evoked by either glucose or K+. In the absence of extracellular Ca2+ there was only a modest stimulation of 45Ca efflux by 5 μM Cd2+. Studies of the ambient free Ca2+ concentration maintained by permeabilized cells also indicate that 5 μM Cd2+ do not mobilize intracellularly bound Ca2+ to any great extent. On the contrary, at this concentration, Cd2+ even suppressed inositol 1,4,5-trisphosphate (IP3)-induced Ca2+ release. The present study suggests that Cd2+ stimulates insulin release by a direct mechanism which does not involve an increase in cytoplasmic free Ca2+ concentration.

Original languageEnglish (US)
Pages (from-to)81-87
Number of pages7
JournalBBA - Molecular Cell Research
Issue number1
StatePublished - Jun 15 1987


  • (Pancreatic β cell)
  • Cadmium ion
  • Calcium channel
  • Inositol trisphosphate
  • Insulin release

ASJC Scopus subject areas

  • Biophysics
  • Cell Biology
  • Molecular Biology


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