released from white adipose tissue ( Donnelly et al . 2005 ). The rest of the lipid stores derive from dietary FAs and de novo lipogenesis. Imbalances between these pathways lead to excessive FA flux and accumulation, which not only induces hepatic (and
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Mohamed Asrih and François R Jornayvaz
Claudia E Robert-Cooperman, Grace C Dougan, Shari L Moak, Mark G Athanason, Melanie N Kuehl, Harris Bell-Temin, Stanley M Stevens Jr, and Brant R Burkhardt
PANTG ( Fig. 6 F, G, H, and I). Therefore, overexpression of PANDER from the pancreatic β-cell decreases hepatic p-AMPK signaling and to a limited extent provides a potential mechanism for the observed increased lipogenesis and gluconeogenesis within
Mingjuan Deng, Fang Qu, Long Chen, Chang Liu, Ming Zhang, Fazheng Ren, Huiyuan Guo, Hao Zhang, Shaoyang Ge, Chaodong Wu, and Liang Zhao
proliferator-activated receptor alpha (PPARa) target genes which are involved in free fatty acid (FFA) oxidation, glycogen storage, thermogenesis, gluconeogenesis, and lipogenesis ( den Besten et al . 2015 ). As such, SCFAs act to both directly and indirectly
Kenshiro Shikano, Eiko Iwakoshi-Ukena, Takaya Saito, Yuki Narimatsu, Atsuki Kadota, Megumi Furumitsu, George E Bentley, Lance J Kriegsfeld, and Kazuyoshi Ukena
protein is Gly-Leu-NH 2 ( Ukena et al. 2014 ), it was named neurosecretory protein GL (NPGL). We have previously shown that chronic infusion of NPGL stimulates food intake and fat accumulation in rats through de novo lipogenesis ( Iwakoshi-Ukena et
David P Macfarlane, Shareen Forbes, and Brian R Walker
lipoprotein particles for transport in the circulation ( Spector 1975 ). The majority of fatty acids in humans are derived from dietary sources and stored as TAGs in adipose tissue, or in small amounts in liver and muscle. De novo lipogenesis (DNL) is an
C G Walker, M C Sugden, G F Gibbons, and M J Holness
mechanism by which glucose metabolism, in particular lipogenesis, is up-regulated in the PPARα null mice is not clear. Although rates of flux through the fatty acid pathway (measured in vivo by 3 H incorporation from 3 H 2 O, which measures total
Felipe de Oliveira Franco, Magno Alves Lopes, Felipe dos Santos Henriques, Rodrigo Xavier das Neves, Cesário Bianchi Filho, and Miguel Luiz Batista Jr
atrophy is caused by (1) increased lipolysis in adipocytes ( Agustsson et al . 2007 , Ryden et al . 2008 , Arner & Langin 2014 ); (2) reduction of lipogenesis ( Ebadi & Mazurak 2014 ); (3) downregulation of adipogenic and lipogenic gene expression
Hyo Youl Moon, Parkyong Song, Cheol Soo Choi, Sung Ho Ryu, and Pann-Ghill Suh
suggested to be critical features ( Browning & Horton 2004 ). Indeed, in HFD-induced hepatic steatosis, both elevated hepatic lipogenesis and impaired lipid oxidation contribute to hepatic TG accumulation ( Postic & Girard 2008 ). Hepatic lipid homeostasis
Melanie Tran, Golam Mostofa, Michael Picard, Jianguo Wu, Li Wang, and Dong-Ju Shin
which is known to promote lipogenesis and insulin resistance underscoring the importance of tissue crosstalk in metabolic dysregulation of NAFLD ( Qureshi & Abrams 2007 , Smith & Kahn 2016 ). Although extensive research has been conducted in the field
Isabel Huang-Doran, Alison Sleigh, Justin J Rochford, Stephen O'Rahilly, and David B Savage
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
