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Luana Lopes Souza
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Aline Cordeiro
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Lorraine Soares Oliveira
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Gabriela Silva Monteiro de Paula
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Larissa Costa Faustino
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Tania Maria Ortiga-Carvalho
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Karen Jesus Oliveira Biophysics Institute Carlos Chagas Filho, Department of Physiology and Pharmacology, Federal University of Rio de Janeiro, Centro de Ciências da Saúde, Avenida Carlos Chagas Filho, 373, Bloco G, Cidade Universitária - Ilha do Fundão, Rio de Janeiro - RJ 21941-902, Brazil

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Carmen Cabanelas Pazos-Moura
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Sobel D Brent GA 2007 A mutant thyroid hormone receptor alpha antagonizes peroxisome proliferator-activated receptor alpha signaling in vivo and impairs fatty acid oxidation . Endocrinology 148 1206 – 1217 . doi:10.1210/en.2006-0836 . Lu

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-11-0142
Volume/Issue:
Volume 211: Issue 1
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Derek Ball School of Life Sciences, Heriot-Watt University, Edinburgh EH14 4AS, UK

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rate of ATP turnover. The lower rate of ATP turnover can be matched by oxidative phosphorylation that employs a combination of glucose/glycogen and fatty acids as the substrates. Early studies demonstrated the balance between fat and carbohydrate

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https://doi.org/10.1530/JOE-14-0408
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Volume 224: Issue 2
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Tina Seidu Department of Physiology and Biophysics, Howard University College of Medicine, Washington, DC, USA

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Patrick McWhorter Department of Chemistry, Youngstown State University, Youngstown, Ohio, USA

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Jessie Myer Department of Biology, University of Missouri, Columbia, Missouri, USA

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Rabita Alamgir Department of Physiology and Biophysics, Howard University College of Medicine, Washington, DC, USA

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Nicole Eregha Department of Physiology and Biophysics, Howard University College of Medicine, Washington, DC, USA

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Dilip Bogle Department of Physiology and Biophysics, Howard University College of Medicine, Washington, DC, USA

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Taylor Lofton Department of Physiology and Biophysics, Howard University College of Medicine, Washington, DC, USA

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Carolyn Ecelbarger Department of Medicine, Georgetown University Medical Center, Washington, DC, USA

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Stanley Andrisse Department of Physiology and Biophysics, Howard University College of Medicine, Washington, DC, USA
Department of Pediatrics, School of Medicine, Johns Hopkins University, Baltimore, Maryland, USA

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utilization (beta-oxidation, colloquially referred to as burning fat), while activation of PPARγ promotes storage (fatty acid synthesis). FxR activation reduced the expression of SREBP1c and activated PPARα ( Watanabe et al. 2004 ). AR has traditionally

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DOI:
https://doi.org/10.1530/JOE-21-0040
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Volume 250: Issue 2
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Sergio Di Meo Department of Biology, University of Naples ‘Federico II’, Naples, Italy

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Susanna Iossa Department of Biology, University of Naples ‘Federico II’, Naples, Italy

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Paola Venditti Department of Biology, University of Naples ‘Federico II’, Naples, Italy

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mitochondrial fatty acid oxidation caused by mitochondrial dysfunction and/or reduced mitochondrial content leads to the accumulation of increased levels of intracellular fatty acyl-CoA and diacylglycerol, which interfere with the insulin signaling ( Lowell

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https://doi.org/10.1530/JOE-16-0598
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Volume 233: Issue 1
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Samuel M Lee Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, University of Illinois at Chicago, Chicago, Illinois, USA

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Jose Muratalla Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, University of Illinois at Chicago, Chicago, Illinois, USA

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Marta Sierra-Cruz Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, University of Illinois at Chicago, Chicago, Illinois, USA

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Jose Cordoba-Chacon Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, University of Illinois at Chicago, Chicago, Illinois, USA

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The first PPAR was identified in 1990 from a cDNA library from mouse liver and was described as a target of hepatocarcinogens that increase the number of peroxisomes and fatty acid oxidation and reduce plasma lipid levels ( Issemann & Green 1990 ). The

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https://doi.org/10.1530/JOE-22-0155
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Volume 257: Issue 1
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A Mostyn
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J C Litten
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K S Perkins
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M C Alves-Guerra
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C Pecqueur
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B Miroux
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M E Symonds
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L Clarke
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mitochondria when fatty acid oxidation predominates: an hypothesis. Experimental Biology and Medicine 226 78 –84. Jekabsons MB , Gregoire FM, Schonfeld-Warden NA, Warden CH & Horwitz BA 1999 T3 stimulates resting metabolism

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https://doi.org/10.1677/joe.1.05448
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Volume 183: Issue 1
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Wanbao Yang Department of Nutrition and Food Science, College of Agriculture and Life Sciences, Texas A&M University, College Station, Texas, USA

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Hui Yan Department of Nutrition and Food Science, College of Agriculture and Life Sciences, Texas A&M University, College Station, Texas, USA

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Quan Pan Department of Nutrition and Food Science, College of Agriculture and Life Sciences, Texas A&M University, College Station, Texas, USA

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James Zheng Shen Department of Nutrition and Food Science, College of Agriculture and Life Sciences, Texas A&M University, College Station, Texas, USA

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Fenghua Zhou Department of Nutrition and Food Science, College of Agriculture and Life Sciences, Texas A&M University, College Station, Texas, USA

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Chaodong Wu Department of Nutrition and Food Science, College of Agriculture and Life Sciences, Texas A&M University, College Station, Texas, USA

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Yuxiang Sun Department of Nutrition and Food Science, College of Agriculture and Life Sciences, Texas A&M University, College Station, Texas, USA

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Shaodong Guo Department of Nutrition and Food Science, College of Agriculture and Life Sciences, Texas A&M University, College Station, Texas, USA

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well. Fatty acid oxidation analysis Isolated primary hepatocytes were seeded into the XF96 cell culture microplate, as mentioned above. 24 h prior to the assay, replace growth medium with substrate-limited medium (DMEM with 0.5 mM glucose, 1mM

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https://doi.org/10.1530/JOE-19-0081
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Volume 241: Issue 3
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Sheree D Martin Metabolic Reprogramming Laboratory, Metabolic Research Unit, School of Medicine and Centre for Molecular and Medical Research, Deakin University, Geelong, Australia

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Sean L McGee Metabolic Reprogramming Laboratory, Metabolic Research Unit, School of Medicine and Centre for Molecular and Medical Research, Deakin University, Geelong, Australia

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, glucose-6-phosphate (G6P), can also enter the pentose phosphate pathway. The oxidative branch of this pathway generates two NADPH molecules, which provide the reductive power required for the generation of new fatty acids through de novo lipogenesis

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https://doi.org/10.1530/JOE-18-0037
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Volume 237: Issue 2
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R Mastrocola Department of Experimental Medicine and Oncology, Section of General Pathology, Corso Raffaello 30, University of Turin, 10125 Turin, Italy
Department of Clinical Pathophysiology, Via Genova 3, University of Turin, 10126 Turin, Italy

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F Restivo Department of Experimental Medicine and Oncology, Section of General Pathology, Corso Raffaello 30, University of Turin, 10125 Turin, Italy
Department of Clinical Pathophysiology, Via Genova 3, University of Turin, 10126 Turin, Italy

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I Vercellinatto Department of Experimental Medicine and Oncology, Section of General Pathology, Corso Raffaello 30, University of Turin, 10125 Turin, Italy
Department of Clinical Pathophysiology, Via Genova 3, University of Turin, 10126 Turin, Italy

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O Danni Department of Experimental Medicine and Oncology, Section of General Pathology, Corso Raffaello 30, University of Turin, 10125 Turin, Italy
Department of Clinical Pathophysiology, Via Genova 3, University of Turin, 10126 Turin, Italy

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E Brignardello Department of Experimental Medicine and Oncology, Section of General Pathology, Corso Raffaello 30, University of Turin, 10125 Turin, Italy
Department of Clinical Pathophysiology, Via Genova 3, University of Turin, 10126 Turin, Italy

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M Aragno Department of Experimental Medicine and Oncology, Section of General Pathology, Corso Raffaello 30, University of Turin, 10125 Turin, Italy
Department of Clinical Pathophysiology, Via Genova 3, University of Turin, 10126 Turin, Italy

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G Boccuzzi Department of Experimental Medicine and Oncology, Section of General Pathology, Corso Raffaello 30, University of Turin, 10125 Turin, Italy
Department of Clinical Pathophysiology, Via Genova 3, University of Turin, 10126 Turin, Italy

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between superoxide and NO, reacts with a variety of molecules, including protein and non-protein-thiols, unsaturated fatty acids and DNA, thus affecting energy conservation mechanisms and oxidative post-translation modification of protein, and ultimately

Article Type:
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DOI:
https://doi.org/10.1677/joe.1.06269
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Volume 187: Issue 1
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Aoife Kiely
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Neville H McClenaghan
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Peter R Flatt
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Philip Newsholme
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normalized and expression of AMPK-P increased from 1 ± 0.59 to 1.75 ± 0.45 units, P = 0.03 (Fig. 5C ), which may indicate higher levels of phosphorylated ACC, resulting in inhibition of fatty acid synthesis and promotion of FA oxidation. In

Article Type:
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https://doi.org/10.1677/JOE-07-0306
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Volume 195: Issue 1
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