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Isabelle Leclerc Division of Diabetes, Endocrinology and Metabolism, Section of Cell Biology, Department of Medicine, Faculty of Medicine, Imperial College London, Sir Alexander Fleming Building, South Kensington Campus, Exhibition Road, SW7 2AZ London, UK

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Guy A Rutter Division of Diabetes, Endocrinology and Metabolism, Section of Cell Biology, Department of Medicine, Faculty of Medicine, Imperial College London, Sir Alexander Fleming Building, South Kensington Campus, Exhibition Road, SW7 2AZ London, UK

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Gargi Meur Division of Diabetes, Endocrinology and Metabolism, Section of Cell Biology, Department of Medicine, Faculty of Medicine, Imperial College London, Sir Alexander Fleming Building, South Kensington Campus, Exhibition Road, SW7 2AZ London, UK

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Nafeesa Noordeen Division of Diabetes, Endocrinology and Metabolism, Section of Cell Biology, Department of Medicine, Faculty of Medicine, Imperial College London, Sir Alexander Fleming Building, South Kensington Campus, Exhibition Road, SW7 2AZ London, UK

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-term storage ( Uyeda & Repa 2006 ). Mice deleted for both alleles of Mlxipl display diminished rates of hepatic glycolysis and lipogenesis resulting in high liver glycogen content, low plasma free fatty acid and reduced adipose tissue mass ( Iizuka et al

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Daniel M Kelly Department of Human Metabolism, Robert Hague Centre for Diabetes and Endocrinology, Medical School, The University of Sheffield, Sheffield S10 2RX, UK

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T Hugh Jones Department of Human Metabolism, Robert Hague Centre for Diabetes and Endocrinology, Medical School, The University of Sheffield, Sheffield S10 2RX, UK
Department of Human Metabolism, Robert Hague Centre for Diabetes and Endocrinology, Medical School, The University of Sheffield, Sheffield S10 2RX, UK

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lipogenesis further increases lipid content and can lead to hepatic steatosis. Impaired insulin action in the adipose tissue allows for increased lipolysis, which additionally promotes re-esterification of lipids in other tissues (such as liver and muscle) and

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Yingning Ji Department of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China

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Wei Liu Department of Nuclear Medicine, Fudan University Shanghai Cancer Center, Shanghai, China

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Yemin Zhu Department of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China

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Yakui Li Department of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China

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Ying Lu Department of Biochemistry and Molecular Biology of School of Basic Medical College of Fudan University, Shanghai, China

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Qi Liu Department of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China

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Lingfeng Tong Department of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China

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Lei Hu Department of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China

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Nannan Xu Department of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China

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Zhangbing Chen Department of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China

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Na Tian Department of Neurology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China

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Lifang Wu Department of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China

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Lian Zhu Department of Laboratory Animal Science, Shanghai Jiao Tong University School of Medicine, Shanghai, China

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Shuang Tang Department of Nuclear Medicine, Fudan University Shanghai Cancer Center, Shanghai, China
Cancer Institute, Fudan University Shanghai Cancer Center, Shanghai, China

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Ping Zhang Department of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China

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Xuemei Tong Department of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China

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de novo lipogenesis ( Townsend & Tseng 2014 , Marlatt & Ravussin 2017 ). Although our previous findings have revealed the role of TKT in limiting lipolysis and fatty acid oxidation in adipose tissues ( Tian et al. 2020 ), the function of TKT in

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Alia H Sukkar Section for Nutrition Research, Department of Medicine, Imperial College London, London, UK

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Aaron M Lett Section for Nutrition Research, Department of Medicine, Imperial College London, London, UK

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Gary Frost Section for Nutrition Research, Department of Medicine, Imperial College London, London, UK

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Edward S Chambers Section for Nutrition Research, Department of Medicine, Imperial College London, London, UK

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substrate for de novo lipogenesis. Propionate enters the TCA cycle as succinyl-CoA, which can be used as a precursor for hepatic gluconeogenesis. The maximum ATP (adenosine triphosphate) yield from complete oxidation of acetate, propionate and butyrate is

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Gencer Sancar German Center for Diabetes Research, Neuherberg, Germany
Department of Internal Medicine IV, Division of Diabetology, Endocrinology and Nephrology, Eberhard-Karls University of Tübingen, Tübingen, Germany
Institute for Diabetes Research and Metabolic Diseases, Helmholtz Center Munich, Eberhard-Karls University of Tübingen, Tübingen, Germany

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Andreas L Birkenfeld German Center for Diabetes Research, Neuherberg, Germany
Department of Internal Medicine IV, Division of Diabetology, Endocrinology and Nephrology, Eberhard-Karls University of Tübingen, Tübingen, Germany
Institute for Diabetes Research and Metabolic Diseases, Helmholtz Center Munich, Eberhard-Karls University of Tübingen, Tübingen, Germany

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novo lipogenesis. Moreover, enhanced lipolysis and decreased lipid storage capacity of the dysfunctional adipose tissue provide FFAs and glycerol that increase re-esterification of TAG, exacerbating hepatosteatosis and liver insulin resistance. DAG

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Liping Luo Department of Metabolism and Endocrinology, Metabolic Syndrome Research Center, Key Laboratory of Diabetes Immunology, National Clinical Research Center for Metabolic Diseases, The Second Xiangya Hospital, 
Central South University, Changsha, Hunan, China

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Meilian Liu Department of Metabolism and Endocrinology, Metabolic Syndrome Research Center, Key Laboratory of Diabetes Immunology, National Clinical Research Center for Metabolic Diseases, The Second Xiangya Hospital, 
Central South University, Changsha, Hunan, China
Department of Biochemistry and Molecular Biology, University of New Mexico Health Sciences Center, 
Albuquerque, New Mexico, USA

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storage organ, adipose tissue stores TGs and releases fatty acids through lipogenesis and lipolysis, respectively. Systemically, feeding stimulates the lipogenic pathway and storage of TGs in the adipose tissue, while fasting induces the activation of

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Shaodong Guo Division of Molecular Cardiology, Department of Medicine, College of Medicine, Texas A&M University Health Science Center, Scott & White, Central Texas Veterans Health Care System, 1901 South 1st Street, Bldg. 205, Temple, Texas 76504, USA

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K) and eukaryotic initiation factor 4E-binding protein (4E-BP), both of which control protein synthesis. Recent data indicate that mTORC1 promotes lipogenesis via the phosphorylation of a phosphatidic acid phosphatase Lipin 1 and nuclear

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Aldo Grefhorst Section of Endocrinology, Department of Internal Medicine, Erasmus MC, University Medical Center Rotterdam, Rotterdam, the Netherlands

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Johanna C van den Beukel Section of Endocrinology, Department of Internal Medicine, Erasmus MC, University Medical Center Rotterdam, Rotterdam, the Netherlands

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Wieneke Dijk Division of Human Nutrition, Nutrition, Metabolism, and Genomics Group, Wageningen University, Wageningen, The Netherlands

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Jacobie Steenbergen Section of Endocrinology, Department of Internal Medicine, Erasmus MC, University Medical Center Rotterdam, Rotterdam, the Netherlands

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Gardi J Voortman Section of Pharmacology, Vascular and Metabolic Diseases, Department of Internal Medicine, Erasmus MC, University Medical Center Rotterdam, Rotterdam, the Netherlands

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Selmar Leeuwenburgh Section of Endocrinology, Department of Internal Medicine, Erasmus MC, University Medical Center Rotterdam, Rotterdam, the Netherlands

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Theo J Visser Section of Endocrinology, Department of Internal Medicine, Erasmus MC, University Medical Center Rotterdam, Rotterdam, the Netherlands

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Sander Kersten Division of Human Nutrition, Nutrition, Metabolism, and Genomics Group, Wageningen University, Wageningen, The Netherlands

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Edith C H Friesema Section of Pharmacology, Vascular and Metabolic Diseases, Department of Internal Medicine, Erasmus MC, University Medical Center Rotterdam, Rotterdam, the Netherlands

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Axel P N Themmen Section of Endocrinology, Department of Internal Medicine, Erasmus MC, University Medical Center Rotterdam, Rotterdam, the Netherlands

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Jenny A Visser Section of Endocrinology, Department of Internal Medicine, Erasmus MC, University Medical Center Rotterdam, Rotterdam, the Netherlands

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lipogenesis has been shown before in liver slices from rats exposed to cold that had a reduced ability to convert 14 C-acetate into 14 C-fatty acids ( Masoro et al. 1957 ). Our data show that the reduced hepatic lipogenesis is the result of the reduced

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Shu-Fang Xia Wuxi School of Medicine, Jiangnan University, Wuxi, China
State Key Laboratory of Food Science and Technology, School of Food Science and Technology, Jiangnan University, Wuxi, China

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Xiao-Mei Duan State Key Laboratory of Food Science and Technology, School of Food Science and Technology, Jiangnan University, Wuxi, China
Shandong Sport Training Center, Jinan, China

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Xiang-Rong Cheng State Key Laboratory of Food Science and Technology, School of Food Science and Technology, Jiangnan University, Wuxi, China

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Li-Mei Chen Wuxi School of Medicine, Jiangnan University, Wuxi, China

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Yan-Jun Kang Wuxi School of Medicine, Jiangnan University, Wuxi, China

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Peng Wang COFCO Corporation Oilseeds Processing Division, Beijing, China

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Xue Tang State Key Laboratory of Food Science and Technology, School of Food Science and Technology, Jiangnan University, Wuxi, China

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Yong-Hui Shi State Key Laboratory of Food Science and Technology, School of Food Science and Technology, Jiangnan University, Wuxi, China

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Guo-Wei Le State Key Laboratory of Food Science and Technology, School of Food Science and Technology, Jiangnan University, Wuxi, China

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. Here, we further investigated part of TH responsive genes that involved in lipogenesis ( Srebp1c , Acc1 , Scd1 and Fasn ), lipid mobilization and fatty acid oxidation genes ( Cpt1α , Lpl and Fabp ), energy metabolism ( Atp5c1 and Cox7c ) and

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T V Novoselova Centre for Endocrinology, Queen Mary University of London, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Charterhouse Square, London, UK

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R Larder University of Cambridge Metabolic Research Laboratories, MRC Metabolic Disease Unit, Wellcome Trust-MRC Institute of Metabolic Science and NIHR Cambridge Biomedical Research Centre, Addenbrooke’s Hospital, Cambridge, UK

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D Rimmington University of Cambridge Metabolic Research Laboratories, MRC Metabolic Disease Unit, Wellcome Trust-MRC Institute of Metabolic Science and NIHR Cambridge Biomedical Research Centre, Addenbrooke’s Hospital, Cambridge, UK

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C Lelliott Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, UK

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E H Wynn Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, UK

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R J Gorrigan Centre for Endocrinology, Queen Mary University of London, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Charterhouse Square, London, UK

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P H Tate Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, UK

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L Guasti Centre for Endocrinology, Queen Mary University of London, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Charterhouse Square, London, UK

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The Sanger Mouse Genetics Project Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, UK

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S O’Rahilly University of Cambridge Metabolic Research Laboratories, MRC Metabolic Disease Unit, Wellcome Trust-MRC Institute of Metabolic Science and NIHR Cambridge Biomedical Research Centre, Addenbrooke’s Hospital, Cambridge, UK

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A J L Clark Centre for Endocrinology, Queen Mary University of London, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Charterhouse Square, London, UK

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D W Logan Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, UK

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A P Coll University of Cambridge Metabolic Research Laboratories, MRC Metabolic Disease Unit, Wellcome Trust-MRC Institute of Metabolic Science and NIHR Cambridge Biomedical Research Centre, Addenbrooke’s Hospital, Cambridge, UK

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L F Chan Centre for Endocrinology, Queen Mary University of London, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Charterhouse Square, London, UK

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state of enzymes involved in lipogenesis and fatty acid synthesis as well as phosphorylation of the rate-limiting enzyme for lipolysis of hormone sensitive lipase (HSL). Phosphorylation of ATP-citrate lyase (ACL), an enzyme responsible for the synthesis

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