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This Article Full Text Full Text (PDF) All Versions of this Article: 286/6/H2243    most recent 00864.2003v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (4) Citing Articles via Google Scholar Google Scholar Articles by Bartelds, B. Articles by van der Leij, F. R. Search for Related Content PubMed PubMed Citation Articles by Bartelds, B. Articles by van der Leij, F. R.

Myocardial carnitine palmitoyltransferase I expression and long-chain fatty acid oxidation in fetal and newborn lambs

¹Department of Pediatrics, University of Groningen, Beatrix Children's Hospital and Research School Guide, 9713 GZ Groningen, The Netherlands; ²Department of Pediatrics, Vanderbilt University Medical Center, Nashville, Tennessee 37232-2495; ³Cellular Biochemistry, Hannah Research Institute, KA6 5ML Scotland, United Kingdom; and ⁴Endocrinology Department, Institut Cochin, Institut National de la Santé et de la Recherche Médicale Unité 567, 75014 Paris, France

Submitted 9 September 2003 ; accepted in final form 27 January 2004

Carnitine palmitoyltransferase I (CPT I) catalyzes the conversion of acyl-CoA to acylcarnitine at the outer mitochondrial membrane and is a key enzyme in the control of long-chain fatty acid (LC-FA) oxidation. Because myocardial LC-FA oxidation increases dramatically after birth, we determined the extent to which CPT I expression contributes to these changes in the perinatal lamb. We measured the steady-state level of transcripts of the CPT1A and CPT1B genes, which encode the liver (L-CPT I) and muscle CPT I (M-CPT I) isoforms, respectively, as well as the amount of these proteins, their total activity, and the amount of carnitine in left ventricular tissue from fetal and newborn lambs. We compared these data with previously obtained myocardial FA oxidation rates in vivo in the same model. The results showed that CPT1B was already expressed before birth and that total CPT I expression transiently increased after birth. The protein level of M-CPT I was high throughout development, whereas that of L-CPT I was only transiently upregulated in the first week after birth. The total CPT I activity in vitro also increased after birth. However, the increase in myocardial FA oxidation measured in vivo (112-fold) by far exceeded the increase in gene expression (2.2-fold), protein amount (1.1-fold), and enzyme activity (1.2-fold) in vitro. In conclusion, these results stress the importance of substrate supply per se in the postnatal increase in myocardial FA oxidation. M-CPT I is expressed throughout perinatal development, making it a primary target for metabolic modulation of myocardial FA oxidation.

cardiac muscle; gene expression; free fatty acid; cardiac metabolism

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