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      Oleate Oxidation and Mitochondrial Substrate Selection in Vascular Smooth Muscle

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          Abstract

          The purpose of this study was to determine the contribution of long-chain fatty acids relative to other mitochondrial substrates in active vascular smooth muscle (VSM). Hog carotid arteries were isometrically contracted in physiological saline solution containing 0.71 m M U-<sup>13</sup>C-oleic acid (bound to albumin at a ratio of 6.8:1), 5 m M 1-<sup>13</sup>C-glucose and 1 m M acetate in the presence or absence of 5 m M carnitine for 6 h at 37°C. Substrate oxidation was determined using <sup>13</sup>C-isotopomer analysis of glutamate. Although oxidation of oleic acid could not be measured at physiological concentrations [0.5 m M (1:1)], oleic acid oxidation was approximately 5% of the total substrates oxidized at the higher concentration examined. Although insignificant, carnitine increased oleic acid oxidation to approximately 8%, and resulted in a decrease in endogenous lipid oxidation, which was 2–12% of the total substrates oxidized. Oxidation of glucose and acetate did not significantly change due to the inclusion of oleic acid in the incubation solutions. Therefore, we conclude that exogenous long-chain fatty acids are minor contributors to substrate oxidation (approximately 5%) in VSM compared to other mitochondrial substrates, such as glucose and acetate, which account for approximately 80% of the substrates oxidized by VSM.

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          Carnitine levels in human serum in health and disease

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            Cytosolic fatty acid binding protein enhances rat hepatocyte [3H]palmitate uptake

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              Author and article information

              Journal
              JVR
              J Vasc Res
              10.1159/issn.1018-1172
              Journal of Vascular Research
              S. Karger AG
              1018-1172
              1423-0135
              2001
              June 2001
              25 May 2001
              : 38
              : 3
              : 276-287
              Affiliations
              Department of Physiology, University of Missouri, Columbia, Mo., USA
              Article
              51056 J Vasc Res 2001;38:276–287
              10.1159/000051056
              11399900
              © 2001 S. Karger AG, Basel

              Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

              Page count
              Figures: 5, References: 34, Pages: 12
              Categories
              Research Paper

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