Effects of Glucose Deprivation or Glucose Instability on Mesangial Cells in Culture

Effects of Glucose Deprivation or Glucose Instability on Mesangial Cells in Culture

Author Santos, Carla de Lima e Autor UNIFESP Google Scholar
Arnoni, Carine P. Autor UNIFESP Google Scholar
Schor, Nestor Autor UNIFESP Google Scholar
Boim, Mirian A. Autor UNIFESP Google Scholar
Institution Universidade Federal de São Paulo (UNIFESP)
Abstract Mesangial cell ( MC) abnormalities play a central role in diabetic nephropathy. Variations in plasma glucose levels may contribute to MC dysfunction. This study evaluated the effects of glucose deprivation or fluctuations on MC viability, glucose uptake, and mesangial matrix production. the expression levels of fibronectin and glucose transporters (GLUT-1 and GLUT-4) were determined. MCs were exposed to normal (NG, 10 m M), low (LG, 1 m M) or high (HG, 30 m M) glucose concentrations for 1, 4, 12, 24 and 72 h. Glucose oscillation was achieved by alternating the glucose concentration (LG, NG or HG) in the medium every 8, 12, and 4 h over a total of 24 h. LG induced a significant increase (90%) in glucose uptake dependent of GLUT-1, which was not followed by alteration in fibronectin expression. Fluctuations in glucose levels induced a rise in glucose uptake also mediated by GLUT-1. Fibronectin did not change in any oscillation group. Results suggest that, in spite of a rise in glucose uptake by MCs under low glucose availability, or exposed to glucose fluctuations, mesangial matrix overproduction did not occur. Thus, neither glucose deprivation nor glucose instability, at least during short periods, is involved in the mesangial matrix overproduction observed in diabetes. Copyright (c) 2008 S. Karger AG, Basel
Keywords Glucose deprivation
Glucose instability
Glucose transporters
Mesangial cell
Diabetic nephropathy
Language English
Date 2009-01-01
Published in American Journal of Nephrology. Basel: Karger, v. 29, n. 3, p. 222-229, 2009.
ISSN 0250-8095 (Sherpa/Romeo, impact factor)
Publisher Karger
Extent 222-229
Origin http://dx.doi.org/10.1159/000156716
Access rights Closed access
Type Article
Web of Science ID WOS:000261132000009
URI http://repositorio.unifesp.br/handle/11600/31215

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