SLC2A2 gene expression in kidney of diabetic rats is regulated by HNF-1 alpha and HNF-3 beta


Autoria(s): FREITAS, H. S.; SCHAAN, B. D.; DAVID-SILVA, A.; SABINO-SILVA, R.; OKAMOTO, M. M.; ALVES-WAGNER, A. B.; MORI, R. C.; MACHADO, U. F.
Contribuinte(s)

UNIVERSIDADE DE SÃO PAULO

Data(s)

20/10/2012

20/10/2012

2009

Resumo

We hypothesize that, in kidney of diabetic rats, hepatocyte nuclear factors (HNF-1 alpha. and HNF-3 beta) play a critical role in the overexpression of solute carrier 2A2 (SLC2A2) gene. Diabetic rats submitted or not to rapid (up to 12 h) and short-term (1, 4 and 6 days) insulin treatment were investigated. Twofold increase in GLUT2 mRNA was observed in diabetic, accompanied by significant increases in HNF-1 alpha and HNF-3 beta expression and binding activity. Additional 2-fold increase in GLUT2 mRNA and HNF-3 beta expression/activity was observed in 12-h insulin-treated rats. Six-day insulin treatment decreased GLUT2 mRNA and HNF-1 alpha expression and activity to levels of non-diabetic rats, whereas HNF-3 beta decreased to levels of non-insulin-treated diabetic rats. Our results provide evidence for a link between the overexpression of SLC2A2 gene and the transcriptional activity of HNF-1 alpha and HNF-3 beta in kidney of diabetic rats. Furthermore, recovery of SLC2A2 gene after 6-day insulin treatment also involves HNF-1 alpha and HNF-3 beta activity. (C) 2009 Elsevier Ireland Ltd. All rights reserved.

Paulo State Foundation[FAPESP02/07384-4]

Paulo State Foundation

Identificador

MOLECULAR AND CELLULAR ENDOCRINOLOGY, v.305, n.1/Fev, p.63-70, 2009

0303-7207

http://producao.usp.br/handle/BDPI/28725

10.1016/j.mce.2009.02.014

http://dx.doi.org/10.1016/j.mce.2009.02.014

Idioma(s)

eng

Publicador

ELSEVIER IRELAND LTD

Relação

Molecular and Cellular Endocrinology

Direitos

restrictedAccess

Copyright ELSEVIER IRELAND LTD

Palavras-Chave #Diabetic nephropathy #GLUT2 #Foxa 2 #EMSA #RENAL PROXIMAL TUBULES #GLUCOSE TRANSPORTERS #GLUT2 GENE #MOLECULAR ADAPTATIONS #INSULIN #CELLS #TRANSCRIPTION #DYSFUNCTION #INHIBITOR #MUTATIONS #Cell Biology #Endocrinology & Metabolism
Tipo

article

original article

publishedVersion