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Published on: November 16, 2011
Mice lacking Ca(v)2.3 (alpha1E) calcium channel exhibit hyperglycemia
1Department of Pharmacology and Neurobiology, Tokyo Medical and Dental University, Tokyo, Japan.
Abstract:
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.
Insights
Calcium voltage-gated channel subfamily 2.3 (Ca(v)2.3) deficiency impairs glucose homeostasis, leading to reduced insulin sensitivity and higher blood glucose levels in mice. These Ca(v)2.3 knockout mice show symptoms similar to non-insulin-dependent diabetes mellitus.
Area of Science:
- Endocrinology
- Physiology
- Molecular Biology
Background:
- Glucose homeostasis is crucial for metabolic health.
- Calcium channels play diverse physiological roles.
- The specific role of Ca(v)2.3 channels in glucose metabolism is not well understood.
Purpose of the Study:
- To elucidate the functional role of the Ca(v)2.3 channel in glucose homeostasis.
- To investigate the impact of Ca(v)2.3 channel deficiency on insulin sensitivity and glucose regulation.
Main Methods:
- In vivo glucose tolerance tests in Ca(v)2.3 knockout (Ca(v)2.3-/-) and wild-type mice.
- In vivo insulin tolerance tests in Ca(v)2.3-/- and wild-type mice.
- Stress-induced glucose release tests in Ca(v)2.3-/- and wild-type mice.
Main Results:
- Ca(v)2.3-/- mice were significantly heavier than wild-type controls.
- Ca(v)2.3-/- mice exhibited significantly higher blood glucose levels during glucose and insulin tolerance tests.
- Stress-induced blood glucose changes were comparable between Ca(v)2.3-/- and wild-type mice.
Conclusions:
- The Ca(v)2.3 channel is implicated in maintaining glucose homeostasis.
- Ca(v)2.3 channel deficiency reduces insulin sensitivity.
- Ca(v)2.3-/- mice display phenotypes consistent with non-insulin-dependent diabetes mellitus.
