Subcellular trafficking of the substrate transporters GLUT4 and CD36 in cardiomyocytes.

Détails

ID Serval
serval:BIB_55A0171467C8
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Titre
Subcellular trafficking of the substrate transporters GLUT4 and CD36 in cardiomyocytes.
Périodique
Cellular and Molecular Life Sciences
Auteur⸱e⸱s
Steinbusch L.K., Schwenk R.W., Ouwens D.M., Diamant M., Glatz J.F., Luiken J.J.
ISSN
1420-9071 (Electronic)
ISSN-L
1420-682X
Statut éditorial
Publié
Date de publication
2011
Volume
68
Numéro
15
Pages
2525-2538
Langue
anglais
Résumé
Cardiomyocytes use glucose as well as fatty acids for ATP production. These substrates are transported into the cell by glucose transporter 4 (GLUT4) and the fatty acid transporter CD36. Besides being located at the sarcolemma, GLUT4 and CD36 are stored in intracellular compartments. Raised plasma insulin concentrations and increased cardiac work will stimulate GLUT4 as well as CD36 to translocate to the sarcolemma. As so far studied, signaling pathways that regulate GLUT4 translocation similarly affect CD36 translocation. During the development of insulin resistance and type 2 diabetes, CD36 becomes permanently localized at the sarcolemma, whereas GLUT4 internalizes. This juxtaposed positioning of GLUT4 and CD36 is important for aberrant substrate uptake in the diabetic heart: chronically increased fatty acid uptake at the expense of glucose. To explain the differences in subcellular localization of GLUT4 and CD36 in type 2 diabetes, recent research has focused on the role of proteins involved in trafficking of cargo between subcellular compartments. Several of these proteins appear to be similarly involved in both GLUT4 and CD36 translocation. Others, however, have different roles in either GLUT4 or CD36 translocation. These trafficking components, which are differently involved in GLUT4 or CD36 translocation, may be considered novel targets for the development of therapies to restore the imbalanced substrate utilization that occurs in obesity, insulin resistance and diabetic cardiomyopathy.
Mots-clé
Animals, Antigens, CD36/metabolism, Fatty Acids/metabolism, Glucose/metabolism, Glucose Transporter Type 4/metabolism, Humans, Intracellular Space/metabolism, Models, Biological, Myocytes, Cardiac/metabolism, Protein Transport
Pubmed
Web of science
Création de la notice
18/07/2013 11:16
Dernière modification de la notice
20/08/2019 15:10
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