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protect against HFD induced obesity by promoting beiging of WAT, which would increase energy expenditure and fatty acid oxidation. Mice fed an HFD supplemented with SCFAs had higher expression of genes related to mitochondrial biogenesis, including Ppargc
Department of Pharmacology, School of Medical Sciences, Diabetes and Obesity Division, St Vincent's Clinical School, Department of Physiology, University of New South Wales, Sydney, New South Wales, Australia
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Department of Pharmacology, School of Medical Sciences, Diabetes and Obesity Division, St Vincent's Clinical School, Department of Physiology, University of New South Wales, Sydney, New South Wales, Australia
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Department of Pharmacology, School of Medical Sciences, Diabetes and Obesity Division, St Vincent's Clinical School, Department of Physiology, University of New South Wales, Sydney, New South Wales, Australia
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. ( doi:10.1073/pnas.0902380106 ) Hoehn KL Turner N Swarbrick MM Wilks D Preston E Phua Y Joshi H Furler SM Larance M Hegarty BD 2010 Acute or chronic upregulation of mitochondrial fatty acid oxidation has no net effect on whole-body energy expenditure or
Hypothalamic Integration Mechanisms, Netherlands Institute for Neuroscience, Amsterdam, The Netherlands
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Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Centre, Leiden, The Netherlands
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Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Centre, Leiden, The Netherlands
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Department of Vascular Medicine, Amsterdam Diabetes Centre, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands
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Hypothalamic Integration Mechanisms, Netherlands Institute for Neuroscience, Amsterdam, The Netherlands
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Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Centre, Leiden, The Netherlands
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Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Centre, Leiden, The Netherlands
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control group in mRNA expression of genes involved in lipid oxidation and the previously reported BA-induced TGR5-D2-UCP1 pathway ( Fig. 6E ). Together these data seem to suggest that tLCA regulates energy expenditure through central bile acid signaling by
Diabetes and Metabolism Division, St Vincent's Clinical School, School of Medical Sciences, School of Biotechnology and Biomolecular Sciences, School of Molecular Bioscience and Sydney Medical School, Garvan Institute of Medical Research, 384 Victoria Street, Darlinghurst, New South Wales 2010, Australia
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Diabetes and Metabolism Division, St Vincent's Clinical School, School of Medical Sciences, School of Biotechnology and Biomolecular Sciences, School of Molecular Bioscience and Sydney Medical School, Garvan Institute of Medical Research, 384 Victoria Street, Darlinghurst, New South Wales 2010, Australia
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Diabetes and Metabolism Division, St Vincent's Clinical School, School of Medical Sciences, School of Biotechnology and Biomolecular Sciences, School of Molecular Bioscience and Sydney Medical School, Garvan Institute of Medical Research, 384 Victoria Street, Darlinghurst, New South Wales 2010, Australia
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Acc2 knockout mice reported a lean phenotype with improved insulin action due to increased whole-body and muscle fatty acid oxidation (FAO) and higher energy expenditure ( Abu-Elheiga et al . 2001 , Abu-Elheiga et al . 2003 , Choi et al . 2007
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Department of Cellular and Integrative Physiology, Section of Nephrology, Department of Internal Medicine, University of Nebraska Medical Center, 985850 Nebraska Medical Center, Omaha, Nebraska 68198-5850, USA
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mice ( Fig. 5 A). The RQ of 0.76 in Parp -KO mice indicates that these mice used fatty acids as the main energy source, while a RQ of 0.82 in WT mice indicated the use of both carbohydrates and fat as their energy source suggesting Parp -KO mice
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total metabolic energy demand ( Morgan et al . 1997 , Bœuf & Payan 2001 ). The primary site of ion exchange is the gill ( Evans et al . 2005 ), which has a low capacity for the oxidation of fatty acids or ketones ( Segner et al . 1997 , Crockett et
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Departments of, Neuroscience, Medicine, Geriatrics, Box 1065, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, New York 10029, USA
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Departments of, Neuroscience, Medicine, Geriatrics, Box 1065, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, New York 10029, USA
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energy expenditure ( Choi et al . 2007 ), or no net effect on energy balance or adiposity ( Hoehn et al . 2010 ), depending on the line analyzed. The latter study ( Hoehn et al . 2010 ) suggests that chronically increased fatty acid oxidation
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Introduction Obesity, which is characterized by abnormal or excessive fat accumulation resulting from energy intake exceeding expenditure, has become a global epidemic and is associated with an array of medical conditions, including insulin
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Jesse Brown Veterans Affairs Medical Center, Chicago, Illinois, USA
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Jesse Brown Veterans Affairs Medical Center, Chicago, Illinois, USA
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-body glucose homeostasis ( Fuller et al. 2015 , Priyadarshini et al. 2015 , Villa et al. 2016 ). Within the adipose tissue, FFA2 has been reported to inhibit insulin-mediated fat accumulation while enhancing energy expenditure and systemic insulin
Centre de Recherche de l’Hôpital Laval, Université Laval, Y2186, 2725 Chemin Ste-Foy, Québec, Canada G1V 4G5
Department of Human Biology, Nutrition and Toxicology Research Institute Maastricht,
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Centre de Recherche de l’Hôpital Laval, Université Laval, Y2186, 2725 Chemin Ste-Foy, Québec, Canada G1V 4G5
Department of Human Biology, Nutrition and Toxicology Research Institute Maastricht,
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Centre de Recherche de l’Hôpital Laval, Université Laval, Y2186, 2725 Chemin Ste-Foy, Québec, Canada G1V 4G5
Department of Human Biology, Nutrition and Toxicology Research Institute Maastricht,
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Centre de Recherche de l’Hôpital Laval, Université Laval, Y2186, 2725 Chemin Ste-Foy, Québec, Canada G1V 4G5
Department of Human Biology, Nutrition and Toxicology Research Institute Maastricht,
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Centre de Recherche de l’Hôpital Laval, Université Laval, Y2186, 2725 Chemin Ste-Foy, Québec, Canada G1V 4G5
Department of Human Biology, Nutrition and Toxicology Research Institute Maastricht,
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Centre de Recherche de l’Hôpital Laval, Université Laval, Y2186, 2725 Chemin Ste-Foy, Québec, Canada G1V 4G5
Department of Human Biology, Nutrition and Toxicology Research Institute Maastricht,
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Centre de Recherche de l’Hôpital Laval, Université Laval, Y2186, 2725 Chemin Ste-Foy, Québec, Canada G1V 4G5
Department of Human Biology, Nutrition and Toxicology Research Institute Maastricht,
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Centre de Recherche de l’Hôpital Laval, Université Laval, Y2186, 2725 Chemin Ste-Foy, Québec, Canada G1V 4G5
Department of Human Biology, Nutrition and Toxicology Research Institute Maastricht,
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Centre de Recherche de l’Hôpital Laval, Université Laval, Y2186, 2725 Chemin Ste-Foy, Québec, Canada G1V 4G5
Department of Human Biology, Nutrition and Toxicology Research Institute Maastricht,
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; other indicators of energy expenditure such as physical activity and heat production, as previously demonstrated in ASP-deficient C3KO mice ( Xia et al. 2002 , 2004 ), were not determined. Nonetheless, the compensatory increase in fatty acid