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Department of Physiology, University of Toronto, Department of Medicine, Mount Sinai Hospital, Toronto General Research Institute and Banting and Best Diabetes Centre, University Health Network, Muscle Health Research Center and Physical Activity and Chronic Disease Unit, Faculty of Health, School of Kinesiology and Health Science, York University, Department of Internal Medicine, University of Manitoba, Medical Sciences Building, 1 King's College Circle, Toronto, Ontario, Canada M5S 1A8
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Department of Physiology, University of Toronto, Department of Medicine, Mount Sinai Hospital, Toronto General Research Institute and Banting and Best Diabetes Centre, University Health Network, Muscle Health Research Center and Physical Activity and Chronic Disease Unit, Faculty of Health, School of Kinesiology and Health Science, York University, Department of Internal Medicine, University of Manitoba, Medical Sciences Building, 1 King's College Circle, Toronto, Ontario, Canada M5S 1A8
Department of Physiology, University of Toronto, Department of Medicine, Mount Sinai Hospital, Toronto General Research Institute and Banting and Best Diabetes Centre, University Health Network, Muscle Health Research Center and Physical Activity and Chronic Disease Unit, Faculty of Health, School of Kinesiology and Health Science, York University, Department of Internal Medicine, University of Manitoba, Medical Sciences Building, 1 King's College Circle, Toronto, Ontario, Canada M5S 1A8
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Introduction Obesity leads to type 2 diabetes mellitus (T2DM) because of insulin resistance, and insulin resistance of obesity is due to elevated circulating levels of free fatty acids (FFAs) and cytokines ( Boden 1997 , Lewis et al . 2002
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hypothesized that an increased de novo lipogenesis after fructose intake in parallel with a decreased fatty acid oxidation leads to hepatic fat deposition. ACC, acetyl-CoA-carboxylase; ATP, adenosine triphosphate; CPT1a, carnitine palmitoyltransferase 1A; FA
Diabetes Institute, Ohio University, Athens, Ohio, USA
Department of Biological Sciences, Ohio University, Athens, Ohio, USA
Molecular & Cellular Biology Program, College of Arts and Sciences, Ohio University, Athens, Ohio, USA
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Diabetes Institute, Ohio University, Athens, Ohio, USA
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Diabetes Institute, Ohio University, Athens, Ohio, USA
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Molecular & Cellular Biology Program, College of Arts and Sciences, Ohio University, Athens, Ohio, USA
Biomedical Engineering Program, Ohio University, Athens, Ohio, USA
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Department of Biomedical Sciences, Ohio University, Athens, Ohio, USA
The Edison Biotechnology Institute, Ohio University, Athens, Ohio, USA
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Diabetes Institute, Ohio University, Athens, Ohio, USA
The Edison Biotechnology Institute, Ohio University, Athens, Ohio, USA
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Diabetes Institute, Ohio University, Athens, Ohio, USA
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Diabetes Institute, Ohio University, Athens, Ohio, USA
Department of Biological Sciences, Ohio University, Athens, Ohio, USA
Molecular & Cellular Biology Program, College of Arts and Sciences, Ohio University, Athens, Ohio, USA
Biomedical Engineering Program, Ohio University, Athens, Ohio, USA
Department of Biomedical Sciences, Ohio University, Athens, Ohio, USA
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patients with NAFLD ( Younossi et al . 2011 ). High-fat (HF) diets promote weight gain leading to an increase in adipose tissue mass (i.e. obesity). Simultaneously, these HF diets cause an increase in levels of circulating free fatty acids (FFAs) and
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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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-induced obesity. Introduction Free fatty acid receptor 2 (FFA2) is a G protein-coupled receptor belonging to the short-chain fatty acid family of receptors. The endogenous ligands for FFA2, short-chain fatty acids (SCFAs), are a group of key metabolites
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transport of docosahexaenoic acid (22:6 n-3, DHA) by GDM ( Herrera & Ortega-Senovilla 2010 , Leveille et al. 2018 ), likely as a consequence of alterations in fatty acids (FA) transport proteins related to phospholipids transfer such as the major
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improvements in metabolic outcomes and GIP may be driven through AT. Humans have different types of AT responsible for regulating whole-body glucose and fatty acid (FA) metabolism, including white adipose tissues and brown adipose tissues (WAT and BAT
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Mary MacKillop Institute for Health Research, Australian Catholic University, Melbourne, Australia
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regulation through several possible mechanisms. Gut microbiota fermentation of dietary fiber produces short-chain fatty acids (SCFAs) that strengthens the gut barrier. SCFAs function as an energy source for intestinal epithelial cells, regulate host immune
Department of Neurosurgery, Graduate School of Medicine, Nippon Medical School, Bunkyo-ku, Tokyo, Japan
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3 , and Pdyn ) and immunohistochemistry (IHC; kisspeptin). The blood samples were utilized for LH, glucose, 3-hydroxybutyrate (3HB), and non-esterified fatty acids (NEFA) assays. All images were captured with a light microscope (BX51; Olympus
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differentiation genes involved in lipid metabolism and lipid transport including glycerol-3-phosphate dehydrogenase (G3PD) and fatty acid-binding protein 4 (FABP4; Hotamisligil et al . 1996 ); many of these genes are regulated by glucocorticoids ( Wu et al
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Department of Pediatrics, School of Medicine, Johns Hopkins University, Baltimore, Maryland, USA
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triglycerides and free fatty acids (FFA), thus driving lipid accumulation mainly in the liver ( Samuel & Shulman 2016 ). Previous work has shown that low-dose DHT female mice displayed obesity-independent impaired glucose tolerance, insulin resistance, and