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In obese Zucker rats, lipids accumulate in the heart despite normal mitochondrial content, morphology and long-chain fatty acid oxidation.
J Physiol 2011; 589(Pt 1):169-80JP

Abstract

We aimed to determine whether an increased rate of long-chain fatty acid (LCFA) transport and/or a reduction in mitochondrial oxidation contributes to lipid deposition in hearts, as lipid accumulation within cardiac muscle has been associated with heart failure. In hearts of lean and obese Zucker rats we examined: (a) triacylglycerol (TAG) and mitochondrial content and distribution using transmission electron microscopy (TEM), (b) LCFA oxidation in cardiac myocytes, and in isolated subsarcolemmal (SS) and intermyofibrillar (IMF) mitochondria, and (c) rates of LCFA transport into cardiac vesicles. Compared to lean rats, in obese Zucker rats, lipid droplet size was similar but there were more (P < 0.05) droplets, and TAG esterification rates and contents were markedly increased. TEM analyses and biochemical determinations showed that SS and IMF mitochondria in obese animals did not appear to be different in their appearance, area, density and number, nor in citrate synthase, β-hydroxy-acyl-CoA dehydrogenase and carnitine palmitoyl-transferase-I enzymatic activities, electron transport chain proteins, nor in their rates of LCFA oxidation either in cardiac myocytes or in isolated SS and IMF mitochondria (P > 0.05). In contrast, sarcolemmal plasma membrane fatty acid binding protein (FABPpm) and fatty acid translocase (FAT/CD36) protein and palmitate transport rates into cardiac vesicles were increased (P < 0.05; +50%) in obese animals. Collectively these data indicate that mitochondrial dysfunction in LCFA oxidation is not responsible for lipid accumulation in obese Zucker rat hearts. Rather, increased sarcolemmal LCFA transport proteins and rates of LCFA transport result in a greater number of lipid droplets within cardiac muscle.

Authors+Show Affiliations

Human Health & Nutritional Sciences, University of Guelph, Guelph, Canada. ghollowa@uoguelph.caNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

21041527

Citation

Holloway, Graham P., et al. "In Obese Zucker Rats, Lipids Accumulate in the Heart Despite Normal Mitochondrial Content, Morphology and Long-chain Fatty Acid Oxidation." The Journal of Physiology, vol. 589, no. Pt 1, 2011, pp. 169-80.
Holloway GP, Snook LA, Harris RJ, et al. In obese Zucker rats, lipids accumulate in the heart despite normal mitochondrial content, morphology and long-chain fatty acid oxidation. J Physiol (Lond). 2011;589(Pt 1):169-80.
Holloway, G. P., Snook, L. A., Harris, R. J., Glatz, J. F., Luiken, J. J., & Bonen, A. (2011). In obese Zucker rats, lipids accumulate in the heart despite normal mitochondrial content, morphology and long-chain fatty acid oxidation. The Journal of Physiology, 589(Pt 1), pp. 169-80. doi:10.1113/jphysiol.2010.198663.
Holloway GP, et al. In Obese Zucker Rats, Lipids Accumulate in the Heart Despite Normal Mitochondrial Content, Morphology and Long-chain Fatty Acid Oxidation. J Physiol (Lond). 2011 Jan 1;589(Pt 1):169-80. PubMed PMID: 21041527.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - In obese Zucker rats, lipids accumulate in the heart despite normal mitochondrial content, morphology and long-chain fatty acid oxidation. AU - Holloway,Graham P, AU - Snook,Laelie A, AU - Harris,Robert J, AU - Glatz,Jan F C, AU - Luiken,Joost J F P, AU - Bonen,Arend, Y1 - 2010/11/01/ PY - 2010/11/3/entrez PY - 2010/11/3/pubmed PY - 2011/4/26/medline SP - 169 EP - 80 JF - The Journal of physiology JO - J. Physiol. (Lond.) VL - 589 IS - Pt 1 N2 - We aimed to determine whether an increased rate of long-chain fatty acid (LCFA) transport and/or a reduction in mitochondrial oxidation contributes to lipid deposition in hearts, as lipid accumulation within cardiac muscle has been associated with heart failure. In hearts of lean and obese Zucker rats we examined: (a) triacylglycerol (TAG) and mitochondrial content and distribution using transmission electron microscopy (TEM), (b) LCFA oxidation in cardiac myocytes, and in isolated subsarcolemmal (SS) and intermyofibrillar (IMF) mitochondria, and (c) rates of LCFA transport into cardiac vesicles. Compared to lean rats, in obese Zucker rats, lipid droplet size was similar but there were more (P < 0.05) droplets, and TAG esterification rates and contents were markedly increased. TEM analyses and biochemical determinations showed that SS and IMF mitochondria in obese animals did not appear to be different in their appearance, area, density and number, nor in citrate synthase, β-hydroxy-acyl-CoA dehydrogenase and carnitine palmitoyl-transferase-I enzymatic activities, electron transport chain proteins, nor in their rates of LCFA oxidation either in cardiac myocytes or in isolated SS and IMF mitochondria (P > 0.05). In contrast, sarcolemmal plasma membrane fatty acid binding protein (FABPpm) and fatty acid translocase (FAT/CD36) protein and palmitate transport rates into cardiac vesicles were increased (P < 0.05; +50%) in obese animals. Collectively these data indicate that mitochondrial dysfunction in LCFA oxidation is not responsible for lipid accumulation in obese Zucker rat hearts. Rather, increased sarcolemmal LCFA transport proteins and rates of LCFA transport result in a greater number of lipid droplets within cardiac muscle. SN - 1469-7793 UR - https://www.unboundmedicine.com/medline/citation/21041527/In_obese_Zucker_rats_lipids_accumulate_in_the_heart_despite_normal_mitochondrial_content_morphology_and_long_chain_fatty_acid_oxidation_ L2 - https://doi.org/10.1113/jphysiol.2010.198663 DB - PRIME DP - Unbound Medicine ER -