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1 Sarah W. Stedman Nutrition & Metabolism Center, Duke University, Durham, North Carolina, United States
2 Exercise and Sport Science, East Carolina University, Greenville, North Carolina, United States; Exercise and Sport Science/Physiology, East Carolina University, 371 Ward Sports Medicine Building, Greenville, North Carolina, 27858, United States
3 Exercise and Sport Science, East Carolina University, Greenville, North Carolina, United States
4 Exercise and Sport Science/Physiology, East Carolina University, 371 Ward Sports Medicine Building, Greenville, North Carolina, 27858, United States
5 Anatomy and Cell Biology, East Carolina University, Greenville, North Carolina, United States
6 Physiology, East Carolina University, Greenville, North Carolina, United States
* To whom correspondence should be addressed. E-mail: cortrightr{at}ecu.edu.
Peroxisomal oxidation yields metabolites that are more efficiently utilized by mitochondria. This is of potential clinical importance as reduced fatty acid oxidation is suspected to promote excess lipid accumulation in obesity-associated insulin resistance. Our purpose was to assess peroxisomal contributions to mitochondrial oxidation in mixed gastrocnemius (MG), liver, and left ventricle (LV) homogenates from lean and fatty (fa/fa) Zucker rats. Results indicate complete mitochondrial oxidation (CO2 production) using various lipid substrates was increased ~2-fold in MG, unaltered in LV, and diminished ~50% in liver of fa/fa rats. In isolated mitochondria, malonyl-CoA inhibited CO2 production from palmitate 78%, whereas adding isolated peroxisomes reduced inhibition to 21%. These data demonstrate peroxisomal products may enter mitochondria independent of CPT-I, thus providing a route to maintain lipid disposal under conditions where malonyl-CoA levels are elevated such as in insulin resistant tissues. Peroxisomal metabolism of lignoceric acid in fa/fa rats was elevated in both liver and MG (LV unaltered), but peroxisomal product distribution varied. A 3-fold elevation in incomplete oxidation was solely responsible for increased hepatic peroxisomal oxidation (CO2 unaltered). Alternatively, only CO2 was detected in MG indicating peroxisomal products were exclusively partitioned to mitochondria for complete lipid disposal. These data suggest tissue-specific destinations for peroxisome-derived products and emphasize a potential role for peroxisomes in skeletal muscle lipid metabolism in the obese, insulin resistant state.
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