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Statins impair glucose uptake in human cells.

Dominika Nowis1, Agata Malenda2, Karolina Furs2

  • 1Department of Immunology , Center of Biostructure Research, Medical University of Warsaw , Warsaw , Poland ; Genomic Medicine, Department of General, Transplant and Liver Surgery , Medical University of Warsaw , Warsaw , Poland.

BMJ Open Diabetes Research & Care
|December 3, 2014
PubMed
Summary

Statins reduce glucose analog uptake in liver, fat, and muscle cells by altering glucose transporter 1 (GLUT1) structure. This cholesterol-dependent mechanism may explain statin-induced hyperglycemia.

Keywords:
GLUT1Glucose UptakePharmacological Therapy

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Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cell Biology

Background:

  • Clinical observations suggest statins can increase blood glucose levels.
  • Understanding the molecular mechanisms behind statin-induced hyperglycemia is crucial for patient management.

Purpose of the Study:

  • To investigate how statins affect glucose analog uptake in human liver, adipose, and skeletal muscle cells.
  • To elucidate the molecular interactions between statins, cholesterol, and glucose transporters.

Main Methods:

  • Utilized flow cytometry and scintillation counting to measure glucose analog uptake in various human cell types.
  • Employed bioinformatics to predict glucose transporter 1 (GLUT1) structure and identify cholesterol-binding motifs.
  • Performed mutagenesis of CRAC motifs and limited proteolysis of GLUT1 to assess statin's molecular effects.

Main Results:

  • Statins significantly inhibited glucose analog uptake across all tested cell types.
  • Cholesterol depletion using methyl-β-cyclodextrin mimicked statin effects, while mevalonic acid or cholesterol supplementation rescued them.
  • Statin treatment induced conformational changes in GLUT1, as evidenced by proteolysis and mutagenesis studies.

Conclusions:

  • Statins impair cellular glucose uptake by inducing cholesterol-dependent conformational changes in glucose transporters (GLUTs).
  • This mechanism provides a molecular explanation for the hyperglycemic side effects observed with statin therapy.