Fatty acid oxidation in cardiac and skeletal muscle mitochondria is unaffected by deletion of CD36

King, Kristen L.; Stanley, William C.; Roșca, Mariana G.; Kerner, János; Hoppel, Charles L.; Febbraio, Maria

doi:10.1016/j.abb.2007.08.020

Cited by 43 publications

(55 citation statements)

References 16 publications

(15 reference statements)

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“…This was observed when they used palmitate (CPT 1 and long-chain acyl-CoA synthase dependent), palmitate-CoA (CPT 1 dependent), or palmitoyl-carnitine (CPT 1 independent) as substrates. Furthermore, a similar decrease in mitochondrial respiration (state 3) was observed when skeletal muscle mitochondria isolated from wild-type mice and CD36 null mice were incubated with SSO, demonstrating that this compound is unspecifi c for FAT/CD36, at least in mitochondria ( 13 ). These fi ndings furthermore suggest that FAT/CD36 might not be essential to preserve mitochondrial ability to oxidize LCFA.…”

Section: Mitochondrial Respiratory Activitysupporting

confidence: 61%

“…These fi ndings suggest a role for FAT/CD36 in mitochondrial fatty acid oxidation independent of CPT 1 ( 3,6 ). In contrast, recent data from King et al ( 13 ) showed no differences in maximal ADPstimulated respiration in mitochondria isolated from skeletal and cardiac muscle from both wild-type and CD36 null mice. This was observed when they used palmitate (CPT 1 and long-chain acyl-CoA synthase dependent), palmitate-CoA (CPT 1 dependent), or palmitoyl-carnitine (CPT 1 independent) as substrates.…”

Section: Mitochondrial Respiratory Activitycontrasting

confidence: 44%

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FAT/CD36 is localized in sarcolemma and in vesicle-like structures in subsarcolemma regions but not in mitochondria

Jeppesen

Mogensen

Prats

et al. 2010

Journal of Lipid Research

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This article is available online at http://www.jlr.org structures in subsarcolemma regions, but not in mitochondria. J. Lipid Res . 2010. 51: 1504-1512. Supplementary key words skeletal muscle • isolated mitochondria • immunocytochemistry • human • Zucker ratsRecent fi ndings in rodent and human skeletal muscle suggest that the plasma membrane protein fatty acid translocase CD36 (FAT/CD36) is located in the mitochondrial outer membrane ( 1-6 ). These fi ndings lead to the idea that FAT/CD36 could be important in regulating longchain fatty acid (LCFA) transport into mitochondria ( 7 ). Elucidating the possible role of mitochondrial FAT/CD36 content could be of great importance, because decreased mitochondrial membrane FAT/CD36 content could reduce mitochondrial LCFA uptake and oxidation, leading to accumulation of LCFA derivatives, which have been linked to the development of insulin resistance by inhibition of key regulatory signaling molecules in the insulin signaling cascade ( 8-10 ). Initially, it was suggested that FAT/CD36 interacted with carnitine palmitoyltransferase 1 (CPT 1), the mitochondrial enzyme that catalyzes the fi rst step in ␤ -oxidation of LCFA, in regulation of LCFA entry into mitochondria. This was based on the observation that the addition of sulfo-N-succinimidyl esters (SSO), a FAT/CD36 inhibitor ( 11, 12 ), reduced CPT 1 activity by ‫ف‬ 50% ( 1 ). However, other studies have shown a ‫ف‬ 90% Abstract The primary aim of the present study was to investigate in which cellular compartments fatty acid translocase CD36 ( FAT/CD36) is localized. Intact and fully functional skeletal muscle mitochondria were isolated from lean and obese female Zucker rats and from 10 healthy male individuals. FAT/CD36 could not be detected in the isolated mitochondria, whereas the mitochondrial marker F 1 ATPase-␤ was clearly detected using immunoblotting. Lack of markers for other membrane structures indicated that the mitochondria were not contaminated with membranes known to contain FAT/CD36. In addition, fl uorescence immunocytochemistry was performed on single muscle fi bers dissected from soleus muscle of lean and obese Zucker rats and from the vastus lateralis muscle from humans. Costaining against FAT/CD36 and MitoNEET clearly show that FAT/CD36 is highly present in sarcolemma and it also associates with some vesicle-like intracellular compartments. However, FAT/CD36 protein was not detected in mitochondrial membranes, supporting the biochemical fi ndings. Based on the presented data, FAT/CD36 seems to be abundantly expressed in sarcolemma and in vesicle-like structures throughout the muscle cell. However, FAT/CD36 is not present in mitochondria in rat or human skeletal muscle. Thus, the functional role of FAT/CD36 in lipid transport seems primarily to be allocated to the plasma membrane in skeletal muscle. -Jeppesen, J., M. Morgensen, C. Prats, K. Sahlin, K. Madsen, and B. Kiens. Abbreviations: CPT 1, carnitine palmitoyltransferase 1; CS, citrate synthase; FABPc, cytosolic fatty acid binding protein; FAT/C...

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Section: Mitochondrial Respiratory Activitysupporting

confidence: 61%

Section: Mitochondrial Respiratory Activitycontrasting

confidence: 44%

FAT/CD36 is localized in sarcolemma and in vesicle-like structures in subsarcolemma regions but not in mitochondria

Jeppesen

Mogensen

Prats

et al. 2010

Journal of Lipid Research

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“…(2007). The final mitochondrial suspension was immediately used for measurement of mitochondrial respiratory parameters.…”

Section: Methodsmentioning

confidence: 99%

Alterations in fatty acid metabolism and sirtuin signaling characterize early type-2 diabetic hearts of fructose-fed rats

et al. 2017

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Despite the fact that skeletal muscle insulin resistance is the hallmark of type‐2 diabetes mellitus (T2DM), inflexibility in substrate energy metabolism has been observed in other tissues such as liver, adipose tissue, and heart. In the heart, structural and functional changes ultimately lead to diabetic cardiomyopathy. However, little is known about the early biochemical changes that cause cardiac metabolic dysregulation and dysfunction. We used a dietary model of fructose‐induced T2DM (10% fructose in drinking water for 6 weeks) to study cardiac fatty acid metabolism in early T2DM and related signaling events in order to better understand mechanisms of disease. In early type‐2 diabetic hearts, flux through the fatty acid oxidation pathway was increased as a result of increased cellular uptake (CD36), mitochondrial uptake (CPT1B), as well as increased β‐hydroxyacyl‐CoA dehydrogenase and medium‐chain acyl‐CoA dehydrogenase activities, despite reduced mitochondrial mass. Long‐chain acyl‐CoA dehydrogenase activity was slightly decreased, resulting in the accumulation of long‐chain acylcarnitine species. Cardiac function and overall mitochondrial respiration were unaffected. However, evidence of oxidative stress and subtle changes in cardiolipin content and composition were found in early type‐2 diabetic mitochondria. Finally, we observed decreased activity of SIRT1, a pivotal regulator of fatty acid metabolism, despite increased protein levels. This indicates that the heart is no longer capable of further increasing its capacity for fatty acid oxidation. Along with increased oxidative stress, this may represent one of the earliest signs of dysfunction that will ultimately lead to inflammation and remodeling in the diabetic heart.

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“…Recently, FAT/CD36 has been found on mitochondrial membranes in rat (14), mouse (30), and human skeletal muscle (4,42). This fatty acid transport protein has been implicated in regulating mitochondrial fatty acid oxidation rates since 1) mitochondrial FAT/CD36 is increased during muscle contraction (14,26), 2) the amount of mitochondrial FAT/CD36 during exercise correlates with mitochondrial function (26), 3) FAT/ CD36 coimmunoprecipitates with CPT I (14,42), and 4) rosiglitazone increases mitochondrial fatty acid oxidation and FAT/ CD36 without altering CPT I activity (2).…”

Section: Discussionmentioning

confidence: 99%

In obese rat muscle transport of palmitate is increased and is channeled to triacylglycerol storage despite an increase in mitochondrial palmitate oxidation

Holloway

Benton²,

Mullen³

et al. 2009

American Journal of Physiology-Endocrinology and Metabolism

137

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Fatty acid oxidation in cardiac and skeletal muscle mitochondria is unaffected by deletion of CD36

Cited by 43 publications

References 16 publications

FAT/CD36 is localized in sarcolemma and in vesicle-like structures in subsarcolemma regions but not in mitochondria

FAT/CD36 is localized in sarcolemma and in vesicle-like structures in subsarcolemma regions but not in mitochondria

Alterations in fatty acid metabolism and sirtuin signaling characterize early type-2 diabetic hearts of fructose-fed rats

In obese rat muscle transport of palmitate is increased and is channeled to triacylglycerol storage despite an increase in mitochondrial palmitate oxidation

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