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        <identifier>oai:hama-med.repo.nii.ac.jp:00002418</identifier>
        <datestamp>2023-08-02T05:01:55Z</datestamp>
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          <dc:title>Changes in the Subcellular Distribution of Free Carnitine and Its Acyl Derivatives in Diabetic Rat Hearts Following Treatment with L-Carnitine</dc:title>
          <dc:creator>Aoshima, Shigeyuki</dc:creator>
          <dc:creator>Fujisawa, Shigeki</dc:creator>
          <dc:creator>Kobayashi, Akira</dc:creator>
          <dc:subject>Free carnitine</dc:subject>
          <dc:subject>Long-chain acylcarnitine</dc:subject>
          <dc:subject>Cellular distribution</dc:subject>
          <dc:subject>Mitochondria</dc:subject>
          <dc:subject>Diabetic heart</dc:subject>
          <dc:subject>L-carnitine treatment</dc:subject>
          <dc:description>Carnitine deficiency has been demonstrated in diabetic hearts, and it is also well known that L-carnitine administration has a beneficial effect on cardiac function. Carnitine treatment would be expected to reduce the accumulation of long-chain acylcarnitine. However, many reports have shown that myocardial long-chain acylcarnitine levels were increased following treatment with L-carnitine in whole-heart studies. Since acylcarnitine exists in both the mitochondrial and cytosolic compartments, it is difficult to investigate changes in subcellular distribution by studying whole-heart preparations. The present study investigated the myocardial subcellular distribution of carnitine and its acyl derivatives in diabetic rats with or without L-carnitine treatment. Approximately 90% of total cellular carnitine was located in the cytosol in the diabetic hearts. Both mitochondrial and cytosolic levels of free carnitine and short-chain acylcarnitine were significantly decreased in the diabetic heart. However, the mitochondrial level of long-chain acylcarnitine was significantly increased. Lcarnitine treatment reduced the mitochondrial level of long-chain acylcarnitine, but the cytosolic level of long-chain acylcarnitine was significantly increased. These results show that L-carnitine treatment prevents the accumulation of long-chain acylcarnitine in the mitochondrial space and then reduces the detergent effect of long-chain acylcarnitine on the mitochondrial membrane. We suggest that it is a possible mechanism of the beneficial effect of L-carnitine treatment on the diabetic heart. (Jpn Heart J 34: 763-772, 1993)</dc:description>
          <dc:description>journal article</dc:description>
          <dc:publisher>International Heart Journal Association</dc:publisher>
          <dc:date>1993-05-10</dc:date>
          <dc:type>VoR</dc:type>
          <dc:format>application/pdf</dc:format>
          <dc:identifier>Japanese Heart Journal</dc:identifier>
          <dc:identifier>6</dc:identifier>
          <dc:identifier>34</dc:identifier>
          <dc:identifier>763</dc:identifier>
          <dc:identifier>772</dc:identifier>
          <dc:identifier>00214868</dc:identifier>
          <dc:identifier>1348673X</dc:identifier>
          <dc:identifier>https://hama-med.repo.nii.ac.jp/record/2418/files/JHeartJ-34-763.pdf</dc:identifier>
          <dc:identifier>http://hdl.handle.net/10271/2483</dc:identifier>
          <dc:identifier>https://hama-med.repo.nii.ac.jp/records/2418</dc:identifier>
          <dc:language>eng</dc:language>
          <dc:relation>10.1536/ihj.34.763</dc:relation>
          <dc:rights>by International Heart Journal Association</dc:rights>
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