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Identification of fatty acid translocase on human skeletal muscle mitochondrial membranes: essential role in fatty acid oxidation

Bezaire, Veronic, Bruce, Clinton R., Heigenhauser, George J. F., Tandon, Narendra N., Glatz, Jan F. C., Luiken, Joost J. J. F., Bonen, Arend and Spriet, Lawrence L. 2006, Identification of fatty acid translocase on human skeletal muscle mitochondrial membranes: essential role in fatty acid oxidation, American journal of physiology : endocrinology and metabolism, vol. 290, no. 3, pp. E509-E515, doi: 10.1152/ajpendo.00312.2005.

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Title Identification of fatty acid translocase on human skeletal muscle mitochondrial membranes: essential role in fatty acid oxidation
Author(s) Bezaire, Veronic
Bruce, Clinton R.ORCID iD for Bruce, Clinton R. orcid.org/0000-0002-0515-3343
Heigenhauser, George J. F.
Tandon, Narendra N.
Glatz, Jan F. C.
Luiken, Joost J. J. F.
Bonen, Arend
Spriet, Lawrence L.
Journal name American journal of physiology : endocrinology and metabolism
Volume number 290
Issue number 3
Start page E509
End page E515
Total pages 7
Publisher American Physiological Society
Place of publication Bethesada, Md.
Publication date 2006
ISSN 0193-1849
1522-1555
Keyword(s) Fatty acid translocase
Long-chain fatty acid
Summary Fatty acid translocase (FAT/CD36) is a transport protein with a high affinity for long-chain fatty acids (LCFA). It was recently identified on rat skeletal muscle mitochondrial membranes and found to be required for palmitate uptake and oxidation. Our aim was to identify the presence and elucidate the role of FAT/CD36 on human skeletal muscle mitochondrial membranes. We demonstrate that FAT/CD36 is present in highly purified human skeletal mitochondria. Blocking of human muscle mitochondrial FAT/CD36 with the specific inhibitor sulfo-N-succimidyl-oleate (SSO) decreased palmitate oxidation in a dose-dependent manner. At maximal SSO concentrations (200 μM) palmitate oxidation was decreased by 95% (P < 0.01), suggesting an important role for FAT/CD36 in LCFA transport across the mitochondrial membranes. SSO treatment of mitochondria did not affect mitochondrial octanoate oxidation and had no effect on maximal and submaximal carnitine palmitoyltransferase I (CPT I) activity. However, SSO treatment did inhibit palmitoylcarnitine oxidation by 92% (P < 0.001), suggesting that FAT/CD36 may be playing a role downstream of CPT I activity, possibly in the transfer of palmitoylcarnitine from CPT I to carnitine-acylcarnitine translocase. These data provide new insight regarding human skeletal muscle mitochondrial fatty acid (FA) transport, and suggest that FAT/CD36 could be involved in the cellular and mitochondrial adaptations resulting in improved and/or impaired states of FA oxidation.
Language eng
DOI 10.1152/ajpendo.00312.2005
Field of Research 119999 Medical and Health Sciences not elsewhere classified
Socio Economic Objective 970111 Expanding Knowledge in the Medical and Health Sciences
HERDC Research category C1.1 Refereed article in a scholarly journal
Persistent URL http://hdl.handle.net/10536/DRO/DU:30067051

Document type: Journal Article
Collections: Faculty of Health
School of Exercise and Nutrition Sciences
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