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Overexpression of carnitine palmitoyltransferase I in skeletal muscle in vivo increases fatty acid oxidation and reduces triacylglycerol esterification

Bruce, Clinton R., Brolin, Camilla, Turner, Nigel, Cleasby, Mark E., van der Leij Feike, R., Cooney, Gregory J. and Kraegen, Edward W. 2007, Overexpression of carnitine palmitoyltransferase I in skeletal muscle in vivo increases fatty acid oxidation and reduces triacylglycerol esterification, American journal of physiology : endocrinology and metabolism, vol. 292, no. 4, pp. E1231-E1237, doi: 10.1152/ajpendo.00561.2006.

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Title Overexpression of carnitine palmitoyltransferase I in skeletal muscle in vivo increases fatty acid oxidation and reduces triacylglycerol esterification
Author(s) Bruce, Clinton R.ORCID iD for Bruce, Clinton R. orcid.org/0000-0002-0515-3343
Brolin, Camilla
Turner, Nigel
Cleasby, Mark E.
van der Leij Feike, R.
Cooney, Gregory J.
Kraegen, Edward W.
Journal name American journal of physiology : endocrinology and metabolism
Volume number 292
Issue number 4
Start page E1231
End page E1237
Total pages 7
Publisher American Physiological Society
Place of publication Bethesada, Md.
Publication date 2007
ISSN 0193-1849
1522-1555
Keyword(s) Mitochondria
Muscle lipids
Substrate metabolism
Summary A key regulatory point in the control of fatty acid (FA) oxidation is thought to be transport of FAs across the mitochondrial membrane by carnitine palmitoyltransferase I (CPT I). To investigate the role of CPT I in FA metabolism, we used in vivo electrotransfer (IVE) to locally overexpress CPT I in muscle of rodents. A vector expressing the human muscle isoform of CPT I was electrotransferred into the right lateral muscles of the distal hindlimb [tibialis cranialis (TC) and extensor digitorum longus (EDL)] of rats, and a control vector expressing GFP was electrotransferred into the left muscles. Initial studies showed that CPT I protein expression peaked 7 days after IVE (+104%, P < 0.01). This was associated with an increase in maximal CPT I activity (+30%, P < 0.001) and a similar increase in palmitoyl-CoA oxidation (+24%; P < 0.001) in isolated mitochondria from the TC. Importantly, oxidation of the medium-chain FA octanoyl-CoA and CPT I sensitivity to inhibition by malonyl-CoA were not altered by CPT I overexpression. FA oxidation in isolated EDL muscle strips was increased with CPT I overexpression (+28%, P < 0.01), whereas FA incorporation into the muscle triacylglycerol (TAG) pool was reduced (−17%, P < 0.01). As a result, intramyocellular TAG content was decreased with CPT I overexpression in both the TC (−25%, P < 0.05) and the EDL (−45%, P < 0.05). These studies demonstrate that acute overexpression of CPT I in muscle leads to a repartitioning of FAs away from esterification and toward oxidation and highlight the importance of CPT I in regulating muscle FA metabolism.
Language eng
DOI 10.1152/ajpendo.00561.2006
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:30067047

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