Gatifloxacin affects GLUT1 gene expression and disturbs glucose homeostasis in vitro

Abstract Gatifloxacin may induce life-threatening dysglycemia. The facilitated glucose transporter type 1 (GLUT1) protein is ubiquitously expressed in many tissues. Disturbed GLUT1 protein function weakens the systemic glycemic control and may cause dysglycemia. In this study we demonstrate that gatifloxacin modulates the transcription and reduces the expression and function of GLUT1 gene in HepG2 cells. When treated with gatifloxacin at concentrations of 3.4 μg/ml (8.4 μM) and 17 μg/ml (42 μM), GLUT1 promoter activity was stimulated by 2.8 and 3.8 folds, GLUT1 mRNA expression was decreased by 41% and 31%, and glucose uptake was decreased by 41% and 52%, respectively. Our findings imply that disturbed GLUT1 gene expression and protein function may underlie the dysglycemic effect of gatifloxacin.