Aminoglycoside antibiotics reduce glucose reabsorption in kidney through down-regulation of SGLT1
| Autor: | Manabu Kawada, Takayuki Usui, Masaaki Ishizuka, Kozo Takamoto, Daishiro Ikeda |
|---|---|
| Rok vydání: | 2003 |
| Předmět: |
medicine.medical_specialty
Monosaccharide Transport Proteins Swine Immunoblotting Biophysics Down-Regulation Biology Kidney Biochemistry Cell Line Nephrotoxicity Mice Sodium-Glucose Transporter 1 In vivo Internal medicine medicine Animals RNA Messenger Molecular Biology Cells Cultured Hexoses Mice Inbred ICR Membrane Glycoproteins urogenital system digestive oral and skin physiology Aminoglycoside Glucose transporter Kidney metabolism Biological Transport Cell Biology Anti-Bacterial Agents Renal glucose reabsorption Aminoglycosides Glucose medicine.anatomical_structure Endocrinology Creatinine Female Gentamicin Gentamicins medicine.drug |
| Zdroj: | Biochemical and Biophysical Research Communications. 308:866-871 |
| ISSN: | 0006-291X |
| DOI: | 10.1016/s0006-291x(03)01502-x |
| Popis: | 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. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect