Titre
CD36 as a target to prevent cardiac lipotoxicity and insulin resistance.
Type
article
Institution
Externe
Auteur(s)
Glatz, J.F.
Auteure/Auteur
Angin, Y.
Auteure/Auteur
Steinbusch, L.K.
Auteure/Auteur
Schwenk, R.W.
Auteure/Auteur
Luiken, J.J.
Auteure/Auteur
Liens vers les personnes
ISSN
1532-2823
Statut éditorial
Publié
Date de publication
2013
Volume
88
Numéro
1
Première page
71
Dernière page/numéro d’article
77
Langue
anglais
Résumé
The fatty acid transporter and scavenger receptor CD36 is increasingly being implicated in the pathogenesis of insulin resistance and its progression towards type 2 diabetes and associated cardiovascular complications. The redistribution of CD36 from intracellular stores to the plasma membrane is one of the earliest changes occurring in the heart during diet induced obesity and insulin resistance. This elicits an increased rate of fatty acid uptake and enhanced incorporation into triacylglycerol stores and lipid intermediates to subsequently interfere with insulin-induced GLUT4 recruitment (i.e., insulin resistance). In the present paper we discuss the potential of CD36 to serve as a target to rectify abnormal myocardial fatty acid uptake rates in cardiac lipotoxic diseases. Two approaches are described: (i) immunochemical inhibition of CD36 present at the sarcolemma and (ii) interference with the subcellular recycling of CD36. Using in vitro model systems of high-fat diet induced insulin resistance, the results indicate the feasibility of using CD36 as a target for adaptation of cardiac metabolic substrate utilization. In conclusion, CD36 deserves further attention as a promising therapeutic target to redirect fatty acid fluxes in the body.
Sujets
PID Serval
serval:BIB_5D5F08CBF06E
PMID
Open Access
Oui
Date de création
2013-07-18T09:18:53.673Z
Date de création dans IRIS
2025-05-20T19:31:53Z