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Aminoglycoside antibiotics reduce glucose reabsorption in kidney through down-regulation of SGLT1

Authors
  • Takamoto, Kozo
  • Kawada, Manabu
  • Usui, Takayuki
  • Ishizuka, Masaaki
  • Ikeda, Daishiro
Type
Published Article
Journal
Biochemical and Biophysical Research Communications
Publisher
Elsevier BV
Publication Date
Jan 01, 2003
Volume
308
Issue
4
Pages
866–871
Identifiers
DOI: 10.1016/S0006-291X(03)01502-X
Source
Elsevier
Keywords
License
Unknown

Abstract

Nephrotoxicity is known to be a major clinical side effect of aminoglycoside antibiotics. Aminoglycosides cause damage to proximal tubular cells in kidney, however the mechanism of toxicity is still unclear. In order to elucidate the mechanism of nephrotoxicity, we studied the effect of aminoglycoside antibiotics on glucose transport systems in vitro and in vivo. As a result, we found that the aminoglycosides significantly reduced Na +/glucose cotransporter (SGLT1)-dependent glucose transport and also down-regulated mRNA and protein levels of the SGLT1 in pig proximal tubular LLC-PK 1 cells. To obtain evidence about SGLT1 down-regulation in vivo, we studied the mRNA expression of SGLT1 using gentamicin C-treated murine kidney and found that gentamicin C down-regulated SGLT1 in vivo as well as in vitro. Furthermore, the gentamicin C-treated mice showed significant rise in urinary glucose excretion. These results indicate that one of the mechanisms of aminoglycoside nephrotoxicity is the down-regulation of SGLT1, which causes reduction in glucose reabsorption in kidney.

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