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Sulfo-N-succinimidyl esters of long chain fatty acids specifically inhibit fatty acid translocase (FAT/CD36)-mediated cellular fatty acid uptake.
Mol Cell Biochem. 2002 Oct; 239(1-2):213-9.MC

Abstract

Sulfo-N-succinimidyl esters of LCFAs are a powerful tool to investigate the functional significance of plasmalemmal proteins in the LCFA uptake process. This notion is based on the following observations. First, sulfo-N-succinimidyl oleate (SSO) was found to inhibit the bulk of LCFA uptake into various cell types, i.e. rat adipocytes, type II pneumocytes and cardiac myocytes. Second, using cardiac giant membrane vesicles, in which LCFA uptake can be investigated in the absence of mitochondrial beta-oxidation, SSO retained the ability to largely inhibit LCFA uptake, indicating that inhibition of LCFA transsarcolemmal transport is its primary action. Third, SSO has no inhibitory effect on glucose and octanoate uptake into giant membrane vesicles derived from heart and skeletal muscle, indicating that its action is specific for LCFA uptake. Finally, SSO specifically binds to the 88 kDa plasmalemmal fatty acid transporter FAT, a rat homologue of human CD36, resulting in an arrest of the transport function of this protein. In addition to its inhibitory action at the plasma membrane level, evidence is presented for the lack of a direct inhibitory effect on subsequent LCFA metabolism. First, the relative contribution of oxidation and esterification to LCFA uptake is not altered in the presence of SSO. Second, isoproterenol-mediated channeling of LCFAs into oxidative pathways is not affected by sulfo-N-succinimidyl palmitate (SSP). As an example of its application, we used SSP to study the role of FAT/CD36 in contraction- and insulin-stimulated LCFA uptake by cardiac myocytes, showing that this transporter is a primary site of regulation of cellular LCFA utilization.

Authors+Show Affiliations

Department of Physiology, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands. S.Coort@fys.unimaas.nlNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

12479588

Citation

Coort, Susan L M., et al. "Sulfo-N-succinimidyl Esters of Long Chain Fatty Acids Specifically Inhibit Fatty Acid Translocase (FAT/CD36)-mediated Cellular Fatty Acid Uptake." Molecular and Cellular Biochemistry, vol. 239, no. 1-2, 2002, pp. 213-9.
Coort SL, Willems J, Coumans WA, et al. Sulfo-N-succinimidyl esters of long chain fatty acids specifically inhibit fatty acid translocase (FAT/CD36)-mediated cellular fatty acid uptake. Mol Cell Biochem. 2002;239(1-2):213-9.
Coort, S. L., Willems, J., Coumans, W. A., van der Vusse, G. J., Bonen, A., Glatz, J. F., & Luiken, J. J. (2002). Sulfo-N-succinimidyl esters of long chain fatty acids specifically inhibit fatty acid translocase (FAT/CD36)-mediated cellular fatty acid uptake. Molecular and Cellular Biochemistry, 239(1-2), 213-9.
Coort SL, et al. Sulfo-N-succinimidyl Esters of Long Chain Fatty Acids Specifically Inhibit Fatty Acid Translocase (FAT/CD36)-mediated Cellular Fatty Acid Uptake. Mol Cell Biochem. 2002;239(1-2):213-9. PubMed PMID: 12479588.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Sulfo-N-succinimidyl esters of long chain fatty acids specifically inhibit fatty acid translocase (FAT/CD36)-mediated cellular fatty acid uptake. AU - Coort,Susan L M, AU - Willems,Jodil, AU - Coumans,Will A, AU - van der Vusse,Ger J, AU - Bonen,Arend, AU - Glatz,Jan F C, AU - Luiken,Joost J F P, PY - 2002/12/14/pubmed PY - 2003/8/9/medline PY - 2002/12/14/entrez SP - 213 EP - 9 JF - Molecular and cellular biochemistry JO - Mol. Cell. Biochem. VL - 239 IS - 1-2 N2 - Sulfo-N-succinimidyl esters of LCFAs are a powerful tool to investigate the functional significance of plasmalemmal proteins in the LCFA uptake process. This notion is based on the following observations. First, sulfo-N-succinimidyl oleate (SSO) was found to inhibit the bulk of LCFA uptake into various cell types, i.e. rat adipocytes, type II pneumocytes and cardiac myocytes. Second, using cardiac giant membrane vesicles, in which LCFA uptake can be investigated in the absence of mitochondrial beta-oxidation, SSO retained the ability to largely inhibit LCFA uptake, indicating that inhibition of LCFA transsarcolemmal transport is its primary action. Third, SSO has no inhibitory effect on glucose and octanoate uptake into giant membrane vesicles derived from heart and skeletal muscle, indicating that its action is specific for LCFA uptake. Finally, SSO specifically binds to the 88 kDa plasmalemmal fatty acid transporter FAT, a rat homologue of human CD36, resulting in an arrest of the transport function of this protein. In addition to its inhibitory action at the plasma membrane level, evidence is presented for the lack of a direct inhibitory effect on subsequent LCFA metabolism. First, the relative contribution of oxidation and esterification to LCFA uptake is not altered in the presence of SSO. Second, isoproterenol-mediated channeling of LCFAs into oxidative pathways is not affected by sulfo-N-succinimidyl palmitate (SSP). As an example of its application, we used SSP to study the role of FAT/CD36 in contraction- and insulin-stimulated LCFA uptake by cardiac myocytes, showing that this transporter is a primary site of regulation of cellular LCFA utilization. SN - 0300-8177 UR - https://www.unboundmedicine.com/medline/citation/12479588/Sulfo_N_succinimidyl_esters_of_long_chain_fatty_acids_specifically_inhibit_fatty_acid_translocase__FAT/CD36__mediated_cellular_fatty_acid_uptake_ L2 - http://ovidsp.ovid.com/ovidweb.cgi?T=JS&PAGE=linkout&SEARCH=12479588.ui DB - PRIME DP - Unbound Medicine ER -