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Nicole M Templeman, Søs Skovsø, Melissa M Page, Gareth E Lim, and James D Johnson

storage in its major peripheral target tissues, primarily by stimulating: (1) glucose uptake in adipose tissue and muscle; (2) glycolysis and glycogen synthesis in muscle and liver; (3) lipogenesis in adipose tissue and liver and (4) protein synthesis in

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Jie Wei, Xia Sun, Yajie Chen, Yuanyuan Li, Liqiong Song, Zhao Zhou, Bing Xu, Yi Lin, and Shunqing Xu

offspring of rats exposed to BPA fed on a HFD compared with controls fed on a HFD. Figure 2 The effect of BPA on hepatic energy metabolism in the liver. (A) mRNA expression of genes associated with lipogenesis, fatty acid oxidation, and gluconeogenesis. (B

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Jaroslav Kuneš, Veronika Pražienková, Andrea Popelová, Barbora Mikulášková, Jana Zemenová, and Lenka Maletínská

decreased de novo lipogenesis owing primarily to negative energy balance due to reduced food intake ( Maletinska et al . 2015 ). Finally, similar results were found in our following study demonstrating that a 2-week-long peripheral treatment of DIO

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Rodrigo Martins Pereira, Kellen Cristina da Cruz Rodrigues, Chadi Pellegrini Anaruma, Marcella Ramos Sant’Ana, Thaís Dantis Pereira de Campos, Rodrigo Stellzer Gaspar, Raphael dos Santos Canciglieri, Diego Gomes de Melo, Rania A Mekary, Adelino Sanchez Ramos da Silva, Dennys Esper Cintra, Eduardo Rochete Ropelle, José Rodrigo Pauli, and Leandro Pereira de Moura

was assessed through analysis of the protein levels and mRNA of CPT1A. Coherently, fasting glycemia presented a positive correlation with hepatic lipogenesis, as assessed by the FAS (fatty acid synthase) content ( Fig. 4F and G , Bioinformatics

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Ken K Y Ho

cost of storage? Indeed, lipogenesis was stimulated during prednisolone treatment ( Fig. 3B ) with the rate of lipid synthesis significantly correlated to energy expenditure after the meal ( Thuzar et al. 2017 ). In short, the enhancement of the non

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Li Zhao, Chunfang Zhu, Meng Lu, Chi Chen, Xiaomin Nie, Buatikamu Abudukerimu, Kun Zhang, Zhiyuan Ning, Yi Chen, Jing Cheng, Fangzhen Xia, Ningjian Wang, Michael D Jensen, and Yingli Lu

percent excess (MPE). Lipidosis and lipogenesis in the liver and different fat depots were calculated by dividing the total concentrations of TG or the corresponding tissue mass by the radioactivity of the corresponding labeled TG, respectively ( Shadid

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Helena A Walz, Linda Härndahl, Nils Wierup, Emilia Zmuda-Trzebiatowska, Fredrik Svennelid, Vincent C Manganiello, Thorkil Ploug, Frank Sundler, Eva Degerman, Bo Ahrén, and Lena Stenson Holst

]sucrose per ml and 1 mM unlabeled 2-deoxy- d -glucose and sucrose. After a 10-min exposure to the isotopes, muscles were immediately frozen in liquid nitrogen and stored at − 80 °C. Insulin-stimulated lipogenesis in white adipocytes

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Abigail Wolf Greenstein, Neena Majumdar, Peng Yang, Papasani V Subbaiah, Rhonda D Kineman, and Jose Cordoba-Chacon

and fibrosis) with TZDs reduces steatosis with variable effects on fibrosis ( Belfort et al . 2006 , Ratziu et al . 2008 , Sanyal et al . 2010 ). The reduction in steatosis is associated with a reduction in hepatic de novo lipogenesis (DNL

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A. H. Cincotta and A. H. Meier


Lipogenesis was determined at two times (07.00 and 16.00 h) during a 14-h daily photoperiod (08.00–22.00 h) in freshly prepared hamster hepatocytes with or without addition of insulin. The hamsters were pretreated for 5 days with bromocriptine (to inhibit prolactin secretion), bromocriptine and prolactin replacement, or control saline injections. Lipogenesis was determined by incorporation of [14C]acetate into total cell lipids over a 30-min interval. Lipogenesis was three times greater at 07.00 than at 16.00 h and insulin was effective in stimulating further lipogenesis only at 07.00 h. Bromocriptine pretreatment severely reduced incorporation of radiolabel at 07.00 h to levels comparable with controls at 16.00 h and completely inhibited the stimulatory effect of insulin at 07.00 h. Prolactin replacement in bromocriptine-treated hamsters reversed the inhibitory effect of bromocriptine on hepatocyte lipogenesis and promoted dramatic lipogenic responses to insulin at 07.00 h. These results indicate that insulin stimulates hepatic lipogenesis only during some portion of a day and that prolactin facilitates the lipogenic response.

J. Endocr. (1985) 106, 173–176

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Meng Guo, Yuna Li, Yan Wang, Zhenkun Li, Xiaohong Li, Peikun Zhao, Changlong Li, Jianyi Lv, Xin Liu, Xiaoyan Du, and Zhenwen Chen

-0051 . eEF1A2 inhibited lipogenesis and lipid use in insulin-resistant skeletal muscle To further uncover the involvement of eEF1A2 in insulin-resistant skeletal muscle, expression levels of the genes of lipogenesis and lipid lipolysis and oxidation