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Department of Pediatrics, School of Medicine, Johns Hopkins University, Baltimore, Maryland, USA
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FFA uptake, de novo lipogenesis (DNL), and/or reduced lipid removal. ( Dowman et al. 2010 , Pettinelli et al. 2011 , Berlanga et al. 2014 ). The development of hepatic steatosis in PCOS is unique due to the influence of HA and is multi
Frontier Science Research Center, Department of Food Science and Human Nutrition, Faculty of Food Science and Nutrition, University of Miyazaki, Miyazaki 889-1692, Japan
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Frontier Science Research Center, Department of Food Science and Human Nutrition, Faculty of Food Science and Nutrition, University of Miyazaki, Miyazaki 889-1692, Japan
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lipogenesis, we evaluated the expression of sterol regulatory element-binding transcription factor 1 (SREBF1), carbohydrate-responsive element-binding protein (ChREBP; MLX1PL), and acetyl-CoA carboxylase (ACC) and the phosphorylation of ACC by using western
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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
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et al . 2005 , Bilz et al . 2006 , Rajasekar & Anuradha 2007 , Nagai et al . 2009 ). In humans, consumption of a fructose-rich diet causes insulin resistance, increases uric acid, and stimulates de novo lipogenesis, resulting in increased
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fat stores is not well known. Fat mass loss can be secondary to an increase in lipolysis and/or a decrease in lipogenesis. Lipolysis in WAT is under hormonal control, where the hormone-sensitive lipase (HSL) is the main regulatory pathway in rodent
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binds to MC4 receptor (MC4R) acts on the opposite way, thereby decreasing food intake and increasing energy expenditure. The adipocyte is a specialised cell that stores excess energy as triacylglycerol (TG) in lipid droplets during lipogenesis. When
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Zurich Center of Integrative Human Physiology (ZIHP), University of Zurich, Zurich, Switzerland
National Center of Competence in Research ‘Kidney.CH’, Zurich, Switzerland
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in lipogenesis, inflammation and secreted adipokines in diet-induced obese Gr fl/fl and Gr ad-ko mice. As shown in Fig. 5A , Gr deletion has a slight or no effects on lipogenic genes as well as adipokines expression. However, pro
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Adiponectin is an adipocyte-derived hormone that has been implicated recently in the regulation of inflammation in immunocytes, and in lipid metabolism and glucose homeostasis in liver, skeletal muscle and adipocytes. However, information in non-rodent models is limited. We have cloned and sequenced the porcine adiponectin open reading frame and evaluated the regulation of adiponectin in vivo following lipopolysaccharide (LPS) or E. coli administration. The porcine sequence shares approximately 88, 86, 85 and 83% homology with the dog, human, cow and mouse adiponectin respectively, and 79-83% similarity with dog, human, cow and mouse proteins at the amino acid level, based on the translated porcine sequence and GenBank submissions for the other species. Relative serum adiponectin concentrations were not altered in pigs infused with E. coli, and mRNA expression in adipose tissue was not responsive to LPS. However, analysis of serum from very lean vs a substantially fatter genotype of pig indicated that relative circulating adiponectin concentrations are higher (P<0.01) in the lean pigs than in the fatter genotype, and that the difference is established relatively early in the growth curve. Also, incubating pig adipocytes for 6 h with recombinant pig adiponectin resulted in an approximately 30% reduction (P<0.05) in lipogenesis compared with adipocytes under basal conditions and with those incubated in the presence of insulin. This is the first report in any species that adiponectin antagonizes the incorporation of glucose carbon into lipid in the adipocyte, and provides additional evidence that adiponectin acts as an autocrine regulatory factor to regulate energy metabolism.
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between the uptake and exportation of fatty acids (which in turn can be esterified or to be oxidized) ( Browning & Horton 2004 , Kawano & Cohen 2013 ). However, when the balance between lipolysis and lipogenesis is altered, or fatty acid influx to the
Department of Functional Genomics, University of Science and Technology, Daejeon, Republic of Korea
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Infectious Disease Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Republic of Korea
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Immunotherapy Convergence Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Republic of Korea
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Immunotherapy Convergence Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Republic of Korea
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Immunotherapy Convergence Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Republic of Korea
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Immunotherapy Convergence Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Republic of Korea
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Department of Biomolecular Science, University of Science and Technology, Daejeon, Republic of Korea
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Department of Biomolecular Science, University of Science and Technology, Daejeon, Republic of Korea
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Immunotherapy Convergence Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Republic of Korea
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. 2013 , Lefterova et al . 2014 ). In adipocytes, PPARγ is required for differentiation, lipogenesis ( Brun et al . 1996 , Tontonoz & Spiegelman 2008 ) and survival ( Imai et al . 2004 ). In addition to its role in adipocyte differentiation and lipid
