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Verapamil inhibits the glucose transport activity of GLUT1

Larry L Louters1, Nathan Stehouwer, Janelle Rekman

  • 1Department of Chemistry & Biochemistry, Calvin College, Grand Rapids, MI, USA.

Journal of Medical Toxicology : Official Journal of the American College of Medical Toxicology
|April 1, 2010
PubMed

Insights

Calcium channel blockers like verapamil can cause hyperglycemia by inhibiting the glucose transporter GLUT1. This effect on glucose uptake is independent of calcium levels and may explain toxicity symptoms.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Pharmacology

Background:

  • Calcium channel blocker (CCB) toxicity is linked to severe hyperglycemia.
  • The precise mechanisms behind CCB-induced hyperglycemia remain unclear.
  • Glucose transporter 1 (GLUT1) mediates basal and stress-induced glucose uptake.

Purpose of the Study:

  • To investigate the impact of the CCB verapamil on GLUT1 glucose uptake activity.
  • To determine if verapamil affects basal and stress-activated GLUT1 transport.

Main Methods:

  • Utilized L929 fibroblast cells and 2-deoxyglucose to measure glucose uptake.
  • Administered varying doses of verapamil to assess dose-dependent effects.
  • Studied verapamil's action under basal and glucose deprivation stress conditions.

Main Results:

  • Verapamil exhibited a dose-dependent inhibition of GLUT1 glucose uptake.
  • Both basal and stress-activated GLUT1 transport were suppressed by verapamil.
  • Inhibition was reversible and dependent on verapamil presence during stress; calcium levels did not influence verapamil's action.

Conclusions:

  • Verapamil directly inhibits GLUT1 transport activity, independent of calcium modulation.
  • This inhibition of GLUT1 may contribute to the hyperglycemia seen in CCB poisoning.
  • Findings offer a novel mechanistic insight into CCB toxicity.

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