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1 University of Guelph
2 Université catholique de Louvain
3 Maastricht University
* To whom correspondence should be addressed. E-mail: abonen{at}uoguelph.ca.
Intramuscular triacylglycerol (IMTG) accumulation in obesity has been attributed to increased fatty acid transport and/or to alterations in mitochondrial fatty acid oxidation. Alternatively, an imbalance in these two processes may channel fatty acids into storage. Therefore, in red and white muscles of lean and obese Zucker rats, we examined whether the increase in IMTG accumulation was attributable to an increased rate of fatty acid transport rather than alterations in subsarcolemmal (SS) or intermyofibrillar IMF) mitochondrial fatty acid oxidation. In obese animals selected parameters were upregulated, including palmitate transport (red; +100%, white; +51%), plasmalemmal FAT/CD36 (red; +116%, white; +115%; not plasmalemmal FABPpm, FATP1 or FATP4), IMTG concentrations (red;~2-fold, white;~4-fold), and mitochondrial content (red +30%). Selected mitochondrial parameters were also greater in obese animals, namely, palmitate oxidation (SS: red; +91%, white; +26%, not IMF mitochondria), FAT/CD36 (SS +65%; IMF +65%), and citrate synthase (SS +19%) and 
-hydroxyacyl-CoA dehydrogenase activities (SS +20%); carnitine palmitoyltransferase-I activity did not differ. Comparing lean and obese rat muscles revealed that the rate of change in IMTG concentration was 8-fold greater than that of fatty acid oxidation (SS mitochondria), when both parameters were expressed relative to fatty transport. Thus, fatty acid transport, esterification and oxidation (SS mitochondria) are upregulated in muscles of obese Zucker rats, with these effects being most pronounced in red muscle. The additional fatty acid taken up is channeled primarily to esterification, suggesting that upregulation in fatty acid transport as opposed to altered fatty acid oxidation is the major determinant of intramuscular lipid accumulation.
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