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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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Institute for Personalized Therapeutic Nutrition, Vancouver, British Columbia, Canada
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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
Institute of Physiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic
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Institute of Physiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic
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University of Chemistry and Technology, Prague, Czech Republic
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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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Department of Social and Administrative Sciences, School of Pharmacy, MCPHS University, Boston, Massachusetts, USA
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Postgraduate Program in Rehabilitation and Functional Performance, Ribeirão Preto Medical School, USP, Ribeirão Preto, São Paulo, Brazil
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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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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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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
Pulmonary/Critical-Care Medicine Branch, NHLBI, National Institutes of Health, Bethesda, Maryland 20892, USA
Department of Medical Physiology, the Panum Institute, DK-2200 Copenhagen, Denmark
Department of Clinical Sciences, Lund, Biomedical Centre, B11, Lund University, SE-221 84 Lund, Sweden
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Pulmonary/Critical-Care Medicine Branch, NHLBI, National Institutes of Health, Bethesda, Maryland 20892, USA
Department of Medical Physiology, the Panum Institute, DK-2200 Copenhagen, Denmark
Department of Clinical Sciences, Lund, Biomedical Centre, B11, Lund University, SE-221 84 Lund, Sweden
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Pulmonary/Critical-Care Medicine Branch, NHLBI, National Institutes of Health, Bethesda, Maryland 20892, USA
Department of Medical Physiology, the Panum Institute, DK-2200 Copenhagen, Denmark
Department of Clinical Sciences, Lund, Biomedical Centre, B11, Lund University, SE-221 84 Lund, Sweden
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Pulmonary/Critical-Care Medicine Branch, NHLBI, National Institutes of Health, Bethesda, Maryland 20892, USA
Department of Medical Physiology, the Panum Institute, DK-2200 Copenhagen, Denmark
Department of Clinical Sciences, Lund, Biomedical Centre, B11, Lund University, SE-221 84 Lund, Sweden
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Pulmonary/Critical-Care Medicine Branch, NHLBI, National Institutes of Health, Bethesda, Maryland 20892, USA
Department of Medical Physiology, the Panum Institute, DK-2200 Copenhagen, Denmark
Department of Clinical Sciences, Lund, Biomedical Centre, B11, Lund University, SE-221 84 Lund, Sweden
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Pulmonary/Critical-Care Medicine Branch, NHLBI, National Institutes of Health, Bethesda, Maryland 20892, USA
Department of Medical Physiology, the Panum Institute, DK-2200 Copenhagen, Denmark
Department of Clinical Sciences, Lund, Biomedical Centre, B11, Lund University, SE-221 84 Lund, Sweden
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Pulmonary/Critical-Care Medicine Branch, NHLBI, National Institutes of Health, Bethesda, Maryland 20892, USA
Department of Medical Physiology, the Panum Institute, DK-2200 Copenhagen, Denmark
Department of Clinical Sciences, Lund, Biomedical Centre, B11, Lund University, SE-221 84 Lund, Sweden
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Pulmonary/Critical-Care Medicine Branch, NHLBI, National Institutes of Health, Bethesda, Maryland 20892, USA
Department of Medical Physiology, the Panum Institute, DK-2200 Copenhagen, Denmark
Department of Clinical Sciences, Lund, Biomedical Centre, B11, Lund University, SE-221 84 Lund, Sweden
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Pulmonary/Critical-Care Medicine Branch, NHLBI, National Institutes of Health, Bethesda, Maryland 20892, USA
Department of Medical Physiology, the Panum Institute, DK-2200 Copenhagen, Denmark
Department of Clinical Sciences, Lund, Biomedical Centre, B11, Lund University, SE-221 84 Lund, Sweden
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Pulmonary/Critical-Care Medicine Branch, NHLBI, National Institutes of Health, Bethesda, Maryland 20892, USA
Department of Medical Physiology, the Panum Institute, DK-2200 Copenhagen, Denmark
Department of Clinical Sciences, Lund, Biomedical Centre, B11, Lund University, SE-221 84 Lund, Sweden
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Pulmonary/Critical-Care Medicine Branch, NHLBI, National Institutes of Health, Bethesda, Maryland 20892, USA
Department of Medical Physiology, the Panum Institute, DK-2200 Copenhagen, Denmark
Department of Clinical Sciences, Lund, Biomedical Centre, B11, Lund University, SE-221 84 Lund, Sweden
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]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
Section of Endocrinology, Diabetes, and Metabolism, Department of Medicine, University of Illinois at Chicago, Chicago, Illinois, USA
Biologic Resources Laboratory, University of Illinois at Chicago, Chicago, Illinois, USA
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Section of Endocrinology, Diabetes, and Metabolism, Department of Medicine, University of Illinois at Chicago, Chicago, Illinois, USA
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Section of Endocrinology, Diabetes, and Metabolism, Department of Medicine, University of Illinois at Chicago, Chicago, Illinois, USA
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Section of Endocrinology, Diabetes, and Metabolism, Department of Medicine, University of Illinois at Chicago, Chicago, Illinois, USA
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Section of Endocrinology, Diabetes, and Metabolism, Department of Medicine, University of Illinois at Chicago, Chicago, Illinois, USA
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Section of Endocrinology, Diabetes, and Metabolism, Department of Medicine, University of Illinois at Chicago, Chicago, Illinois, USA
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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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ABSTRACT
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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-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