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J. Biol. Chem., Vol. 280, Issue 10, 9265-9271, March 11, 2005

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Peroxisomal and Mitochondrial Oxidation of Fatty Acids in the Heart, Assessed from the ¹³C Labeling of Malonyl-CoA and the Acetyl Moiety of Citrate^*

Fang Bian, Takhar Kasumov, Katherine R. Thomas, Kathryn A. Jobbins, France David, Paul E. Minkler, Charles L. Hoppel, and Henri Brunengraber¶

From the Departments of Nutrition and Pharmacology, Case Western Reserve University, Cleveland Ohio 44106

We previously showed that a fraction of the acetyls used to synthesize malonyl-CoA in rat heart derives from partial peroxisomal oxidation of very long and long-chain fatty acids. The ¹³C labeling ratio (malonyl-CoA)/(acetyl moiety of citrate) was >1.0 with ¹³C-fatty acids, which yields [¹³C]acetyl-CoA in both mitochondria and peroxisomes and < 1.0 with substrates, which yields [¹³C]acetyl-CoA only in mitochondria. In this study, we tested the influence of ¹³C-fatty acid concentration and chain length on the labeling of acetyl-CoA formed in mitochondria and/or peroxisomes. Hearts were perfused with increasing concentrations of labeled docosanoate, oleate, octanoate, hexanoate, butyrate, acetate, or dodecanedioate. In contrast to the liver, peroxisomal oxidation of 1-¹³C-fatty acids in heart does not form [1-¹³C]acetate. With [1-¹³C]docosanoate and [1,12-¹³C₂]dodecanedioate, malonyl-CoA enrichment plateaued at 11 and 9%, respectively, with no detectable labeling of the acetyl moiety of citrate. Thus, in the intact rat heart, docosanoate and dodecanedioate appear to be oxidized only in peroxisomes. With [1-¹³C]oleate or [1-¹³C]octanoate, the labeling ratio >1 indicates the partial peroxisomal oxidation of oleate and octanoate. In contrast, with [3-¹³C]octanoate, [1-¹³C]hexanoate, [1-¹³C]butyrate, or [1,2-¹³C₂]acetate, the labeling ratio was <0.7 at all concentrations. Therefore, in rat heart, (i) n-fatty acids shorter than 8 carbons do not undergo peroxisomal oxidation, (ii) octanoate undergoes only one cycle of peroxisomal -oxidation, (iii) there is no detectable transfer to the mitochondria of acetyl-CoA from the cytosol or the peroxisomes, and (iv) the capacity of C₂–C₁₈ fatty acids to generate mitochondrial acetyl-CoA decreases with chain length.

Received for publication, November 12, 2004 , and in revised form, December 14, 2004.

^* This work was supported by Grants RO1DK035543 and 2PO1AG015885 from the National Institutes of Health and by the Cleveland Mt. Sinai Health Care Foundation. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

^¶ To whom correspondence should be addressed: Dept. of Nutrition, Case Western Reserve University, 10900 Euclid Ave., Cleveland OH 44106-4906. Tel.: 216-368-6429; E-mail: hxb8{at}case.edu.

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