e-ISSN 1694-2078
p-ISSN 1694-2086

Arch Med Biomed Res. 2014;1:66-78.

Florence Boyer1, Philippe Rondeau1, Emmanuel Bourdon1

Author Affiliations

1Groupe d'Etude sur l'Inflammation Chronique et l'Obésité (GEICO), Structure fédérative Environnement Biodiversité Santé-FED4126, Université de La Réunion, Plateforme CYROI, 15, avenue René Cassin – BP 7151, 97715 Saint Denis Messag Cedex 09, La Réunion, France

correspondence to
Emmanuel Bourdon; Emmanuel.bourdon@univ-reunion.fr

Received: April 23, 2014
Revised: May 15, 2014
Accepted: May 16, 2014


The high level of oxidative stress in obesity-linked type 2 diabetes is associated with elevated formation of advanced glycation end products (AGEs). Given that very little is known about the role of proteasome and AGE receptors (CD36 and RAGE) and ligands (HMGB1) in adipocyte response to hyperglycemia-induced oxidative stress, this study was focused on assessing the impact of either chronic or intermittent hyperglycemia on proteasome expression and activity, RAGE and CD36 expressions and HMGB1 mRNA levels in SW872 cell lines. 15% and 80% increases in ROS production and carbonyl accumulation were observed, respectively, when cells were incubated in hyperglycemic conditions compared to the control. Enhanced immunoproteasome expression was observed by Western blot attesting the inflammatory situation of SW872 cells when incubated in chronic hyperglycemia. Using fluorescent specific substrates, significant enhanced trypsin like activity of the proteasome (+60%) were observed in cells incubated in hyperglycemic conditions. Chronic hyperglycemia leads to cellular protein damages to a greater extent than intermittent hyperglycemia induced. An increase in CD36 and RAGE expressions was shown in SW872 treated in hyperglycemic conditions. Using real time quantitative PCR, enhanced HMGB1 mRNA expressions were evidenced in hyperglycemic-treated SW872 cell line. Our data clearly indicate that hyperglycemia treatments result in an increase in oxidative damage in SW872 cell lines that may affect its functionality. Oxidative stress drives the activation of inflammatory processes though RAGE ligands and receptors that can perturb insulin signalling leading to glucose intolerance and diabetes.

KEY WORDS: Diabetes; Oxidative stress; Proteasome; Adipocytes

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