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Isabel Huang-Doran Metabolic Research Laboratories, Wolfson Brain Imaging Centre, Institute of Metabolic Science

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Alison Sleigh Metabolic Research Laboratories, Wolfson Brain Imaging Centre, Institute of Metabolic Science

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Justin J Rochford Metabolic Research Laboratories, Wolfson Brain Imaging Centre, Institute of Metabolic Science

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Stephen O'Rahilly Metabolic Research Laboratories, Wolfson Brain Imaging Centre, Institute of Metabolic Science

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David B Savage Metabolic Research Laboratories, Wolfson Brain Imaging Centre, Institute of Metabolic Science

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indicate that these proteins possess functions in addition to their proposed roles in lipogenesis. Lipid droplet assembly Central to the adipocyte's role as a fat storage organ is the ability to store lipid species in an inert form within the cell as a

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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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Moe Thuzar Endocrine Hypertension Research Centre, University of Queensland Frazer Institute and Princess Alexandra Hospital, Brisbane, Queensland, Australia
Department of Endocrinology & Diabetes, Princess Alexandra Hospital, Brisbane, Queensland, Australia

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Muthanna Abdul Halim Endocrine Hypertension Research Centre, University of Queensland Frazer Institute and Princess Alexandra Hospital, Brisbane, Queensland, Australia

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Michael Stowasser Endocrine Hypertension Research Centre, University of Queensland Frazer Institute and Princess Alexandra Hospital, Brisbane, Queensland, Australia

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of cardiovascular tissue, promoting proinflammatory phenotypes in immune cells, and dysfunction of adipocytes (reduced thermogenesis, increased lipogenesis, adipogenesis, and inflammation). In these non-epithelial tissues, cortisol can also activate

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