Please use this identifier to cite or link to this item: https://hdl.handle.net/10316/11789
Title: Impaired glucose transporter-1 degradation and increased glucose transport and oxidative stress in response to high glucose in chondrocytes from osteoarthritic versus normal human cartilage
Authors: Rosa, Susana C. 
Gonçalves, Juliana 
Judas, Fernando 
Mobasheri, Ali 
Lopes, Celeste 
Mendes, Alexandrina Ferreira 
Keywords: diabetes mellitus; osteoartrite
Issue Date: 2-Jun-2009
Publisher: BioMedCentral
Citation: ROSA, Susana C. et al. - Impaired glucose transporter-1 degradation and increased glucose transport and oxidative stress in response to high glucose in chondrocytes from osteoarthritic versus normal human cartilage. Arthritis Research & Therapy Vol 11 No 3.R80
Abstract: Introduction Disorders that affect glucose metabolism, namely diabetes mellitus (DM), may favor the development and/or progression of osteoarthritis (OA). Thus far, little is known regarding the ability of chondrocytes to adjust to variations in the extracellular glucose concentration, resulting from hypoglycemia and hyperglycemia episodes, and so, to avoid deleterious effects resulting from deprivation or intracellular accumulation of glucose. The aim of this study was to compare the ability of normal and OA chondrocytes to regulate their glucose transport capacity in conditions of insufficient or excessive extracellular glucose and to identify the mechanisms involved and eventual deleterious consequences, namely the production of reactive oxygen species (ROS).
URI: https://hdl.handle.net/10316/11789
DOI: 10.1186/ar2713
Rights: openAccess
Appears in Collections:FFUC- Artigos em Revistas Internacionais

Files in This Item:
File Description SizeFormat
AR&T_2009.pdf1.45 MBAdobe PDFView/Open
Show full item record

SCOPUSTM   
Citations

163
checked on Nov 4, 2024

WEB OF SCIENCETM
Citations

143
checked on Nov 2, 2024

Page view(s) 50

494
checked on Nov 5, 2024

Download(s)

239
checked on Nov 5, 2024

Google ScholarTM

Check

Altmetric

Altmetric


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.