Accumulation of cadmium in pancreatic β cells is similar to that of calcium in being stimulated by both glucose and high potassium

Thomas Nilsson, Fredrik Rorsman, Per Olof Berggren, Bo Hellman

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

The transport of Cd2+ and the effects of this ion on secretory activity and metabolism were investigated in β cell-rich pancreatic islets isolated from obese-hyperglycemic mice. The endogenous cadmium content was 2.5 μmol/kg dry wt. After 60 min of incubation in a Ca2+-deficient medium containing 2.5 μM Cd2+ the islet cadmium content increased to 0.18 mmol/kg dry wt. This uptake was reduced by approx. 50% in the presence of 1.28 mM Ca2+. The incorporation of Cd2+ was stimulated either by raising the concentration of glucose to 20 mM or K+ to 30.9 mM. Whereas D-600 suppressed the stimulatory effect of glucose by 75%, it completely abolished that obtained with high K+. Only about 40% of the incorporated cadmium was mobilized during 60 min of incubation in a Cd2+-free medium containing 0.5 mM EGTA. It was possible to demonstrate a glucose-induced suppression of Cd2+ efflux into a Ca2+-deficient medium. Concentrations of Cd2+ up to 2.5 μM did not affect glucose oxidation, whereas, there was a progressive inhibition when the Cd2+ concentration was above 10 μM. Basal insulin release was stimulated by 5 μM Cd2+. At a concentration of 160 μM, Cd2+ did not affect basal insulin release but significantly inhibited the secretory response to glucose. It is concluded that the β cell uptake of Cd2+ is facilitated by the activation of voltage-dependent Ca2+ channels. Apparently, the accumulation of Cd2+ mimics that of Ca2+ also involving a component of intracellular sequestration promoted by glucose.

Original languageEnglish
Pages (from-to)270-277
Number of pages8
JournalBBA - Molecular Cell Research
Volume888
Issue number3
DOIs
StatePublished - Oct 10 1986
Externally publishedYes

Fingerprint

Cadmium
Potassium
Calcium
Glucose
Obese Mice
Insulin
Gallopamil
Egtazic Acid
Islets of Langerhans
Ions

Keywords

  • (Pancreatic β cell)
  • Cadmium accumulation
  • Insulin secretion
  • Stimulus-secretion coupling

ASJC Scopus subject areas

  • Biophysics
  • Cell Biology
  • Molecular Biology

Cite this

Accumulation of cadmium in pancreatic β cells is similar to that of calcium in being stimulated by both glucose and high potassium. / Nilsson, Thomas; Rorsman, Fredrik; Berggren, Per Olof; Hellman, Bo.

In: BBA - Molecular Cell Research, Vol. 888, No. 3, 10.10.1986, p. 270-277.

Research output: Contribution to journalArticle

Nilsson, Thomas ; Rorsman, Fredrik ; Berggren, Per Olof ; Hellman, Bo. / Accumulation of cadmium in pancreatic β cells is similar to that of calcium in being stimulated by both glucose and high potassium. In: BBA - Molecular Cell Research. 1986 ; Vol. 888, No. 3. pp. 270-277.
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abstract = "The transport of Cd2+ and the effects of this ion on secretory activity and metabolism were investigated in β cell-rich pancreatic islets isolated from obese-hyperglycemic mice. The endogenous cadmium content was 2.5 μmol/kg dry wt. After 60 min of incubation in a Ca2+-deficient medium containing 2.5 μM Cd2+ the islet cadmium content increased to 0.18 mmol/kg dry wt. This uptake was reduced by approx. 50{\%} in the presence of 1.28 mM Ca2+. The incorporation of Cd2+ was stimulated either by raising the concentration of glucose to 20 mM or K+ to 30.9 mM. Whereas D-600 suppressed the stimulatory effect of glucose by 75{\%}, it completely abolished that obtained with high K+. Only about 40{\%} of the incorporated cadmium was mobilized during 60 min of incubation in a Cd2+-free medium containing 0.5 mM EGTA. It was possible to demonstrate a glucose-induced suppression of Cd2+ efflux into a Ca2+-deficient medium. Concentrations of Cd2+ up to 2.5 μM did not affect glucose oxidation, whereas, there was a progressive inhibition when the Cd2+ concentration was above 10 μM. Basal insulin release was stimulated by 5 μM Cd2+. At a concentration of 160 μM, Cd2+ did not affect basal insulin release but significantly inhibited the secretory response to glucose. It is concluded that the β cell uptake of Cd2+ is facilitated by the activation of voltage-dependent Ca2+ channels. Apparently, the accumulation of Cd2+ mimics that of Ca2+ also involving a component of intracellular sequestration promoted by glucose.",
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