Add time:10/01/2019         Source:infona.pl

Peptide-hormone secretion is partially triggered by Ca 2+ influx through voltage-gated Ca 2+ channels (VGCCs) and gene inactivation of Zn 2+ -sensitive Ca v 2.3-type VGCCs is associated with disturbed glucose homeostasis in mice. Zn 2+ has been implicated in pancreatic islet cell crosstalk and recent findings indicate that sudden cessation of Zn 2+ supply during hypoglycemia triggers glucagon secretion in rodents. Here we show that diethyldithiocarbamate (DEDTC), a chelating agent for Zn 2+ and other group IIB metal ions, differentially affects blood glucose and serum peptide hormone level in wild-type mice and mice lacking the Ca v 2.3-subunit. Fasting glucose and glucagon level were significantly higher in Ca v 2.3-deficient compared to wild-type mice, while DEDTC Zn 2+ -chelation produced a significant and correlated increase of blood glucose and serum glucagon concentration in wild-type but not Ca v 2.3-deficient mice. Glucose tolerance tests revealed severe glucose intolerance in Zn 2+ -depleted Ca v 2.3-deficient but not vehicle-treated Ca v 2.3-deficient or Zn 2+ -depleted wildtype mice. Collectively, these findings indicate that Ca v 2.3 channels are critically involved in the Zn 2+ -mediated suppression of glucagon secretion during hyperglycemia. Especially under conditions of Zn 2+ deficiency, ablation or dysfunction of Ca v 2.3 channels may lead to severe disturbances in glucose homeostasis.

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