The effect of malonyl-coa on fatty acid oxidation in rat muscle and liver mitochondria |
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| Affiliation: | 1. Unidad de Endocrinología Pediátrica, Hospital General Universitario de Ciudad Real, Ciudad Real, España;2. Unidad de Endocrinología Pediátrica, Hospital Clínico Universitario de Valladolid, Valladolid, España;3. Unidad de Endocrinología Pediátrica, Hospital Clínico Universitario Lozano Blesa, Zaragoza, España;4. Unidad de Endocrinología Pediátrica, Hospital Universitario Sant Joan de Reus, Reus, Tarragona, España;5. Unidad de Metabolismo Infantil, Hospital Universitario Reina Sofía - IMIBIC, Universidad de Córdoba, Córdoba, España;6. Departamento Materno Infantil y Radiología. U.G.C. de Pediatría, Hospital Universitario Puerta del Mar, Universidad de Cádiz, Cádiz, España;7. Unidad de Endocrinología Pediátrica, Complejo Hospitalario Universitario de Albacete, Albacete, España;8. Unidad de Endocrinología Pediátrica, Hospital Universitario de Cruces Baracaldo, Vizcaya, España;1. Department of Hepatobiliary Surgery and Institute of Advanced Surgical Technology and Engineering, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an, Shaanxi Province, China;2. National-Local Joint Engineering Research Center for Precision Surgery & Regenerative Medicine, Xi’an Jiaotong University, Xi’an, Shaanxi Province, China;3. Department of Vascular Surgery, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an, Shaanxi Province, China;4. Department of Surgery, Division of Surgical Oncology, The Ohio State University Wexner Medical Center and James Comprehensive Cancer Center, Columbus, Ohio, USA;5. School of Automation Science and Engineering, Faculty of Electronic and Information Engineering, Xi''an Jiaotong University, China;6. Genome Institute, The First Affiliated Hospital of Xi''an Jiaotong University, China;7. Institute of Digestive Disease and Department of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Shatin, Hong Kong, China;1. Complex Systems Unit, Aalto University School of Science, P.O. Box 12200, FI-00076, Finland;2. Robert Bosch LLC, Palo Alto, CA 94304, USA;3. Mechanisms and Design Lab, Hewlett Packard Enterprise Labs, Palo Alto, CA, USA;1. Jiangsu Key Laboratory of Advanced Catalytic Materials and Technology, School of Petrochemical Engineering, Changzhou University, Changzhou 213164, PR China;2. College of Chemical Engineering, Beijing University of Chemical Technology, Beijing 100029, PR China;3. Changzhou Institute of Advanced Materials, Beijing University of Chemical Technology, Changzhou 213164, PR China;4. Key Laboratory of Advanced Reactor Engineering and Safety, Ministry of Education, Tsinghua University, Beijing 100084, PR China;1. Departamento de Ciencias de la Atmósfera y los Océanos, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Buenos Aires, Argentina;2. Consejo Nacional de Investigaciones Científicas y Técnicas, Buenos Aires, Argentina;3. Departamento Oceanografía, Servicio de Hidrografía Naval, Buenos Aires, Argentina;4. Expérimentation et Approches Numériques, Laboratoire d’Océanographie et du Climat, Université Pierre et Marie Curie, Paris, France |
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| Abstract: | The effect of malonyl-CoA on palmitate oxidation was compared for skeletal muscle and liver mitochondria from fed rats and rats starved for 18 and 42 h. The nutritional state did not influence the palmitate oxidation rate by both types of mitochondria. Muscle mitochondria are more sensitive to malonyl-CoA inhibition of palmitate oxidation than are liver mitochondria. Their response is not influenced by the nutritional state, in contrast to that of liver mitochondria. The extent of inhibition was not dependent on the carnitine concentration (above 0.5 mM), but higher at lower palmitate:albumin ratio or palmitate concentration. |
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