Mice lacking Ca(v)2.3 (alpha1E) calcium channel exhibit hyperglycemia

Biochem Biophys Res Commun. 2001 Dec 14;289(4):791-5. doi: 10.1006/bbrc.2001.6051.


To investigate the functional role of Ca(v)2.3 channel in glucose homeostasis, we performed in vivo glucose tolerance and insulin tolerance tests together with stress-induced glucose release tests using mice deficient in Ca(v)2.3 channel (Ca(v)2.3-/-). The Ca(v)2.3-/- mice were significantly heavier than wild-type mice. In glucose tolerance and insulin tolerance tests, Ca(v)2.3-/- mice showed a significantly higher blood glucose level compared to wild-type mice. However, stress-induced blood glucose changes in Ca(v)2.3-/- mice were similar to those in wild-type mice. These results suggest that Ca(v)2.3 channel plays a role in glucose homeostasis by reducing insulin sensitivity and that Ca(v)2.3-/- mice exhibit symptoms resembling non-insulin-dependent diabetes mellitus.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blood Glucose / metabolism
  • Calcium Channels / deficiency*
  • Calcium Channels / genetics*
  • Calcium Channels / metabolism
  • Calcium Channels, R-Type
  • Cation Transport Proteins*
  • Cold Temperature / adverse effects
  • Diabetes Mellitus, Type 2 / etiology
  • Diabetes Mellitus, Type 2 / genetics
  • Diabetes Mellitus, Type 2 / metabolism
  • Disease Models, Animal
  • Glucose Tolerance Test
  • Homeostasis
  • Hyperglycemia / etiology*
  • Hyperglycemia / metabolism*
  • Immobilization / adverse effects
  • Insulin / administration & dosage
  • Insulin / blood
  • Mice
  • Mice, Knockout
  • Stress, Physiological / blood


  • Blood Glucose
  • Cacna1e protein, mouse
  • Calcium Channels
  • Calcium Channels, R-Type
  • Cation Transport Proteins
  • Insulin