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

Details

Serval ID
serval:BIB_55A0171467C8
Type
Article: article from journal or magazin.
Publication sub-type
Review (review): journal as complete as possible of one specific subject, written based on exhaustive analyses from published work.
Collection
Publications
Title
Subcellular trafficking of the substrate transporters GLUT4 and CD36 in cardiomyocytes.
Journal
Cellular and Molecular Life Sciences
Author(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
Publication state
Published
Issued date
2011
Volume
68
Number
15
Pages
2525-2538
Language
english
Abstract
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.
Keywords
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
Create date
18/07/2013 10:16
Last modification date
20/08/2019 14:10
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