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4. Dual regulation of TxNIP by ChREBP and FoxO1 in liver

Author

Noblet, Benedicte, Benhamed, Fadila, O-Sullivan, InSug, Zhang, Wenwei, Filhoulaud, Gaëlle, Montagner, Alexandra, Polizzi, Arnaud, Marmier, Solenne, Burnol, Anne-Françoise, Guilmeau, Sandra, Issad, Tarik, Guillou, Hervé, Bernard, Catherine, Unterman, Terry, and Postic, Catherine

Published
2021
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5. La O-GlcNAc transférase

Author

Parlati, Lucia, primary, Regnier, Marion, additional, Benhamed, Fadila, additional, Issad, Tarik, additional, and Postic, Catherine, additional

Published
2024
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7. Corrigendum to “O-GlcNAc transferase acts as a critical nutritional node for the control of liver homeostasis” [JHEP Reports 6 [2024] 100878]

Author

Ortega-Prieto, Paula, Parlati, Lucia, Benhamed, Fadila, Regnier, Marion, Cavalcante, Isadora, Montabord, Mélanie, Onifarasoaniaina, Rachel, Favier, Maryline, Pavlovic, Natasa, Magusto, Julie, Cauzac, Michèle, Pagesy, Patrick, Gautheron, Jérémie, Desdouets, Chantal, Guilmeau, Sandra, Issad, Tarik, and Postic, Catherine

Published
2024
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8. A Specific ChREBP and PPARα Cross-Talk Is Required for the Glucose-Mediated FGF21 Response

Author

Iroz, Alison, Montagner, Alexandra, Benhamed, Fadila, Levavasseur, Françoise, Polizzi, Arnaud, Anthony, Elodie, Régnier, Marion, Fouché, Edwin, Lukowicz, Céline, Cauzac, Michèle, Tournier, Emilie, Do-Cruzeiro, Marcio, Daujat-Chavanieu, Martine, Gerbal-Chalouin, Sabine, Fauveau, Véronique, Marmier, Solenne, Burnol, Anne-Françoise, Guilmeau, Sandra, Lippi, Yannick, Girard, Jean, Wahli, Walter, Dentin, Renaud, Guillou, Hervé, and Postic, Catherine

Published
2017
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9. Interaction between hormone-sensitive lipase and ChREBP in fat cells controls insulin sensitivity

Author

Morigny, Pauline, Houssier, Marianne, Mairal, Aline, Ghilain, Claire, Mouisel, Etienne, Benhamed, Fadila, Masri, Bernard, Recazens, Emeline, Denechaud, Pierre-Damien, Tavernier, Geneviève, Caspar-Bauguil, Sylvie, Virtue, Sam, Sramkova, Veronika, Monbrun, Laurent, Mazars, Anne, Zanoun, Madjid, Guilmeau, Sandra, Barquissau, Valentin, Beuzelin, Diane, Bonnel, Sophie, Marques, Marie, Monge-Roffarello, Boris, Lefort, Corinne, Fielding, Barbara, Sulpice, Thierry, Astrup, Arne, Payrastre, Bernard, Bertrand-Michel, Justine, Meugnier, Emmanuelle, Ligat, Laetitia, Lopez, Frédéric, Guillou, Hervé, Ling, Charlotte, Holm, Cecilia, Rabasa-Lhoret, Remi, Saris, Wim H. M., Stich, Vladimir, Arner, Peter, Rydén, Mikael, Moro, Cedric, Viguerie, Nathalie, Harms, Matthew, Hallén, Stefan, Vidal-Puig, Antonio, Vidal, Hubert, Postic, Catherine, and Langin, Dominique

Published
2019
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10. Molecular phenomics and metagenomics of hepatic steatosis in non-diabetic obese women

Author

Hoyles, Lesley, Fernández-Real, José-Manuel, Federici, Massimo, Serino, Matteo, Abbott, James, Charpentier, Julie, Heymes, Christophe, Luque, Jèssica Latorre, Anthony, Elodie, Barton, Richard H., Chilloux, Julien, Myridakis, Antonis, Martinez-Gili, Laura, Moreno-Navarrete, José Maria, Benhamed, Fadila, Azalbert, Vincent, Blasco-Baque, Vincent, Puig, Josep, Xifra, Gemma, Ricart, Wifredo, Tomlinson, Christopher, Woodbridge, Mark, Cardellini, Marina, Davato, Francesca, Cardolini, Iris, Porzio, Ottavia, Gentileschi, Paolo, Lopez, Frédéric, Foufelle, Fabienne, Butcher, Sarah A., Holmes, Elaine, Nicholson, Jeremy K., Postic, Catherine, Burcelin, Rémy, and Dumas, Marc-Emmanuel

Published
2018
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13. ATGL-dependent white adipose tissue lipolysis controls hepatocyte PPARα activity

Author

Fougerat, Anne, Schoiswohl, Gabriele, Polizzi, Arnaud, Régnier, Marion, Wagner, Carina, Smati, Sarra, Fougeray, Tiffany, Lippi, Yannick, Lasserre, Frederic, Raho, Ilyès, Melin, Valentine, Tramunt, Blandine, Métivier, Raphaël, Sommer, Caroline, Benhamed, Fadila, Alkhoury, Chantal, Greulich, Franziska, Jouffe, Céline, Emile, Anthony, Schupp, Michael, Gourdy, Pierre, Dubot, Patricia, Levade, Thierry, Meynard, Delphine, Ellero-Simatos, Sandrine, Gamet-Payrastre, Laurence, Panasyuk, Ganna, Uhlenhaut, Henriette, Amri, Ez-Zoubir, Cruciani-Guglielmacci, Céline, Postic, Catherine, Wahli, Walter, Loiseau, Nicolas, Montagner, Alexandra, Langin, Dominique, Lass, Achim, and Guillou, Hervé

Published
2022
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14. Nuclear HMGB1 protects from nonalcoholic fatty liver disease through negative regulation of liver X receptor

Author

Personnaz, Jean, primary, Piccolo, Enzo, additional, Dortignac, Alizée, additional, Iacovoni, Jason S., additional, Mariette, Jérôme, additional, Rocher, Vincent, additional, Polizzi, Arnaud, additional, Batut, Aurélie, additional, Deleruyelle, Simon, additional, Bourdens, Lucas, additional, Delos, Océane, additional, Combes-Soia, Lucie, additional, Paccoud, Romain, additional, Moreau, Elsa, additional, Martins, Frédéric, additional, Clouaire, Thomas, additional, Benhamed, Fadila, additional, Montagner, Alexandra, additional, Wahli, Walter, additional, Schwabe, Robert F., additional, Yart, Armelle, additional, Castan-Laurell, Isabelle, additional, Bertrand-Michel, Justine, additional, Burlet-Schiltz, Odile, additional, Postic, Catherine, additional, Denechaud, Pierre-Damien, additional, Moro, Cédric, additional, Legube, Gaelle, additional, Lee, Chih-Hao, additional, Guillou, Hervé, additional, Valet, Philippe, additional, Dray, Cédric, additional, and Pradère, Jean-Philippe, additional

Published
2022
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15. ChREBPβ is dispensable for the control of glucose homeostasis and energy balance

Author

Recazens, Emeline, primary, Tavernier, Geneviève, additional, Dufau, Jérémy, additional, Bergoglio, Camille, additional, Benhamed, Fadila, additional, Cassant-Sourdy, Stéphanie, additional, Marques, Marie-Adeline, additional, Caspar-Bauguil, Sylvie, additional, Brion, Alice, additional, Monbrun, Laurent, additional, Dentin, Renaud, additional, Ferrier, Clara, additional, Leroux, Mélanie, additional, Denechaud, Pierre-Damien, additional, Moro, Cedric, additional, Concordet, Jean-Paul, additional, Postic, Catherine, additional, Mouisel, Etienne, additional, and Langin, Dominique, additional

Published
2022
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16. Liver PPARα is crucial for whole-body fatty acid homeostasis and is protective against NAFLD

Author

Montagner, Alexandra, Polizzi, Arnaud, Fouché, Edwin, Ducheix, Simon, Lippi, Yannick, Lasserre, Frédéric, Barquissau, Valentin, Régnier, Marion, Lukowicz, Céline, Benhamed, Fadila, Iroz, Alison, Bertrand-Michel, Justine, Al Saati, Talal, Cano, Patricia, Mselli-Lakhal, Laila, Mithieux, Gilles, Rajas, Fabienne, Lagarrigue, Sandrine, Pineau, Thierry, Loiseau, Nicolas, Postic, Catherine, Langin, Dominique, Wahli, Walter, and Guillou, Hervé

Published
2016
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17. The lipogenic transcription factor ChREBP dissociates hepatic steatosis from insulin resistance in mice and humans

Author

Benhamed, Fadila, Denechaud, Pierre-Damien, Lemoine, Maud, Robichon, Celine, Moldes, Marthe, Bertrand-Michel, Justine, Ratziu, Vlad, Serfaty, Lawrence, Housset, Chantal, Capeau, Jacqueline, Girard, Jean, Guillou, Herve, and Postic, Catherine

Subjects
Insulin resistance -- Diagnosis -- Care and treatment, Liver -- Physiological aspects, Transcription factors -- Properties, Health care industry
Abstract

Nonalcoholic fatty liver disease (NAFLD) is associated with all features of the metabolic syndrome. Although deposition of excess triglycerides within liver cells, a hallmark of NAFLD, is associated with a loss of insulin sensitivity, it is not clear which cellular abnormality arises first. We have explored this in mice overexpressing carbohydrate responsive element-binding protein (ChREBP). On a standard diet, mice overexpressing ChREBP remained insulin sensitive, despite increased expression of genes involved in lipogenesis/fatty acid esterification and resultant hepatic steatosis (simple fatty liver). Lipidomic analysis revealed that the steatosis was associated with increased accumulation of monounsaturated fatty acids (MUFAs). In primary cultures of mouse hepatocytes, ChREBP overexpression induced expression of stearoyl-CoA desaturase 1 (Scd1), the enzyme responsible for the conversion of saturated fatty acids (SFAs) into MUFAs. SFA impairment of insulin-responsive Akt phosphorylation was therefore rescued by the elevation of Scd1 levels upon ChREBP overexpression, whereas pharmacological or shRNA-mediated reduction of Scd1 activity decreased the beneficial effect of ChREBP on Akt phosphorylation. Importantly, ChREBP-overexpressing mice fed a high-fat diet showed normal insulin levels and improved insulin signaling and glucose tolerance compared with controls, despite having greater hepatic steatosis. Finally, ChREBP expression in liver biopsies from patients with non-alcoholic steatohepatitis was increased when steatosis was greater than 50% and decreased in the presence of severe insulin resistance. Together, these results demonstrate that increased ChREBP can dissociate hepatic steatosis from insulin resistance, with beneficial effects on both glucose and lipid metabolism., Introduction Nonalcoholic fatty liver disease (NAFLD) is gaining increasing recognition as a component of the epidemic of obesity worldwide. NAFLD is the most common cause of liver dysfunction and affects [...]

Published
2012
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18. Salt-inducible kinase 2 links transcriptional coactivator p300 phosphorylation to the prevention of ChREBP-dependent hepatic steatosis in mice

Author

Bricambert, Julien, Miranda, Jonatan, Benhamed, Fadila, Girard, Jean, Postic, Catherine, and Dentin, Renaud

Subjects
Fatty liver -- Genetic aspects -- Development and progression, Phosphorylation -- Observations, Genetic transcription -- Physiological aspects, Health care industry
Abstract

Obesity and type 2 diabetes are associated with increased lipogenesis in the liver. This results in fat accumulation in hepatocytes, a condition known as hepatic steatosis, which is a form of nonalcoholic fatty liver disease (NAFLD), the most common cause of liver dysfunction in the United States. Carbohydrate-responsive element- binding protein (ChREBP), a transcriptional activator of glycolytic and lipogenic genes, has emerged as a major player in the development of hepatic steatosis in mice. However, the molecular mechanisms enhancing its transcriptional activity remain largely unknown. In this study, we have identified the histone acetyltransferase (HAT) coactivator p300 and serine/threonine kinase salt-inducible kinase 2 (SIK2) as key upstream regulators of ChREBP activity. In cultured mouse hepatocytes, we showed that glucose-activated p300 acetylated ChREBP on Lys672 and increased its transcriptional activity by enhancing its recruitment to its target gene promoters. SIK2 inhibited p300 HAT activity by direct phosphorylation on Ser89, which in turn decreased ChREBP-mediated lipogenesis in hepatocytes and mice overexpressing SIK2. Moreover, both liver-specific SIK2 knockdown and p300 overexpression resulted in hepatic steatosis, insulin resistance, and inflammation, phenotypes reversed by SIK2/p300 co-overexpression. Finally, in mouse models of type 2 diabetes and obesity, low SIK2 activity was associated with increased p300 HAT activity, ChREBP hyperacetylation, and hepatic steatosis. Our findings suggest that inhibition of hepatic p300 activity may be beneficial for treating hepatic steatosis in obesity and type 2 diabetes and identify SIK2 activators and specific p300 inhibitors as potential targets for pharmaceutical intervention., Introduction The metabolic syndrome, which represents a collection of abnormalities including obesity, type 2 diabetes, dyslipidemia, fatty liver, and a proinflammatory state (1), affects more than 27% of adults in [...]

Published
2010
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19. Hepatic gene regulation by glucose and polyunsaturated fatty acids: a role for ChREBP

Author

Dentin, Renaud, Denechaud, Pierre-Damien, Benhamed, Fadila, Girard, Jean, and Postic, Catherine

Subjects
Glycogen -- Synthesis, Genetic research, Blood sugar, Gene expression, Carbohydrate metabolism, Triglycerides, Unsaturated fatty acids, Food/cooking/nutrition
Abstract

The liver is a major site for carbohydrate metabolism (glycolysis and glycogen synthesis) and triglyceride synthesis (lipogenesis). In the last decade, increasing evidence has emerged to show that nutrients, in particular, glucose and fatty acids, are able to regulate hepatic gene expression in a transcriptional manner. Indeed, although insulin was long thought to be the major regulator of hepatic gene expression, it is now clear that glucose metabolism rather that glucose itself also contributes substantially to the coordinated regulation of carbohydrate and lipid homeostasis in liver. In fact, the recent discovery of the glucose-signaling transcription factor carbohydrate responsive element binding protein (ChREBP) shed some light on the molecular mechanisms by which glycolytic and lipogenic genes are reciprocally regulated by glucose and fatty acids in liver. Here, we will review some of the recent studies that have begun to elucidate the regulation and function of this key transcription factor in liver. Indeed, a better understanding of the mechanisms by which glucose and fatty acids control hepatic gene expression may provide novel insight into the development of new therapeutic strategies for a better management of diseases involving blood glucose and/or disorders of lipid metabolism. KEY WORDS: * ChREBP * glucose * polyunsaturated fatty acids * transcriptional regulation * glycolytic and lipogenic gene expression

Published
2006

20. Nuclear HMGB1 protects from non-alcoholic fatty liver diseases through negative regulation of liver X receptor

Author

Personnaz, Jean, primary, Piccolo, Enzo, additional, Dortignac, Alizée, additional, Iacovoni, Jason S., additional, Mariette, Jérôme, additional, Polizzi, Arnaud, additional, Batut, Aurélie, additional, Deleruyelle, Simon, additional, Paccoud, Romain, additional, Moreau, Elsa, additional, Martins, Frédéric, additional, Clouaire, Thomas, additional, Benhamed, Fadila, additional, Montagner, Alexandra, additional, Wahli, Walter A., additional, Schwabe, Robert F., additional, Yart, Armelle, additional, Castan-Laurell, Isabelle, additional, Postic, Catherine, additional, Moro, Cédric, additional, Legube, Gaelle, additional, Lee, Chih-Hao, additional, Guillou, Hervé, additional, Valet, Philippe, additional, Dray, Cédric, additional, and Pradère, Jean-Philippe, additional

Published
2021
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23. O-GlcNacylation Links TxNIP to Inflammasome Activation in Pancreatic β Cells

Author

Filhoulaud, Gaelle, Benhamed, Fadila, Pagesy, Patrick, Bonner, Caroline, Fardini, Yann, Ilias, Anissa, Movassat, Jamileh, Burnol, Anne-Francoise, Guilmeau, Sandra, Kerr-Conte, Julie, Pattou, François, Issad, Tarik, Postic, Catherine, Institut Cochin (IC UM3 (UMR 8104 / U1016)), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Recherche translationnelle sur le diabète - U 1190 (RTD), Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Unité de Biologie Fonctionnelle et Adaptative (BFA (UMR_8251 / U1133)), Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Université Sorbonne Paris Cité (USPC), [Institut Cochin] Département Endocrinologie, métabolisme, diabète (EMD) (EMD), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), ANR-17-CE14-0027,LYSODIABETES,Régulation de la fonction lysosomale par les nutriments dans le diabète de type 2(2017), Issad, Tarik, Du gène à la physiopathologie, des maladies rares aux maladies communes - O-GlcNAc-glycosylation des facteurs de transcription FoxO1 et ChREBP : Implication dans le phénomène de glucotoxicité - - DIAB-O-GLYC2008 - ANR-08-GENO-0008 - GENOPAT - VALID, This work was supported by grants from ANR (Agence Nationale de la Recherche, Grant Diab-O-Glyc), FRM (Foundation for the Medical Research, DEQ20150331744), ARD (Association de Recherche sur le Diabète), and the SFD (Société Francophone du Diabète)., and ANR-08-GENO-0008,DIAB-O-GLYC,O-GlcNAc-glycosylation des facteurs de transcription FoxO1 et ChREBP : Implication dans le phénomène de glucotoxicité(2008)

Subjects
[SDV.MHEP.EM] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism, Endocrinology, O-GlcNAcylation, inflammasome, Endocrinology, Diabetes and Metabolism, [SDV]Life Sciences [q-bio], [SDV.BBM] Life Sciences [q-bio]/Biochemistry, Molecular Biology, TXNIP (thioredoxin-interacting protein), [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, hyperglycemia, [SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism, pancreatic beta cells, Original Research
Abstract

International audience; Thioredoxin interacting protein (TxNIP), which strongly responds to glucose, has emerged as a central mediator of glucotoxicity in pancreatic β cells. TxNIP is a scaffold protein interacting with target proteins to inhibit or stimulate their activity. Recent studies reported that high glucose stimulates the interaction of TxNIP with the inflammasome protein NLRP3 (NLR family, pyrin domain containing 3) to increase interleukin-1 β (IL1β) secretion by pancreatic β cells. To better understand the regulation of TxNIP by glucose in pancreatic β cells, we investigated the implication of O-linked β-N-acetylglucosamine (O-GlcNAcylation) in regulating TxNIP at the posttranslational level. O-GlcNAcylation of proteins is controlled by two enzymes: the O-GlcNAc transferase (OGT), which transfers a monosaccharide to serine/threonine residues on target proteins, and the O-GlcNAcase (OGA), which removes it. Our study shows that TxNIP is subjected to O-GlcNAcylation in response to high glucose concentrations in β cell lines. Modification of the O-GlcNAcylation pathway through manipulation of OGT or OGA expression or activity significantly modulates TxNIP O-GlcNAcylation in INS1 832/13 cells. Interestingly, expression and O-GlcNAcylation of TxNIP appeared to be increased in islets of diabetic rodents. At the mechanistic level, the induction of the O-GlcNAcylation pathway in human and rat islets promotes inflammasome activation as evidenced by enhanced cleaved IL1β. Overexpression of OGT in HEK293 or INS1 832/13 cells stimulates TxNIP and NLRP3 interaction, while reducing TxNIP O-GlcNAcylation through OGA overexpression destabilizes this interaction. Altogether, our study reveals that O-GlcNAcylation represents an important regulatory mechanism for TxNIP activity in β cells.

Published
2019
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27. Hepatokines in metabolic disease: novel insights into FGF21 regulation by glucose

Author

Postic, Catherine, Iroz, Alison, Montagner, Alexandra, Benhamed, Fadila, Polizzi, Arnaud, Levavasseur, Françoise, Anthony, E., WAHLI, Walter, Dentin, Renaud, Guillou, Hervé, Centre National de la Recherche Scientifique (CNRS), ToxAlim (ToxAlim), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National Polytechnique (Toulouse) (Toulouse INP), Université Fédérale Toulouse Midi-Pyrénées-Ecole Nationale Vétérinaire de Toulouse (ENVT), Institut National Polytechnique (Toulouse) (Toulouse INP), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Ecole d'Ingénieurs de Purpan (INPT - EI Purpan), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Recherche Agronomique (INRA), Toxicologie Intégrative & Métabolisme (ToxAlim-TIM), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Recherche Agronomique (INRA)-Université Toulouse III - Paul Sabatier (UT3), Institut Cochin (UMR_S567 / UMR 8104), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), and ProdInra, Migration

Subjects
[SDV.TOX] Life Sciences [q-bio]/Toxicology, [SDV.TOX]Life Sciences [q-bio]/Toxicology, ComputingMilieux_MISCELLANEOUS
Abstract

International audience

Published
2018

28. Interaction between hormone-sensitive lipase and ChREBP in fat cells controls insulin sensitivity

Author

Morigny, Pauline, primary, Houssier, Marianne, additional, Mairal, Aline, additional, Ghilain, Claire, additional, Mouisel, Etienne, additional, Benhamed, Fadila, additional, Masri, Bernard, additional, Recazens, Emeline, additional, Denechaud, Pierre-Damien, additional, Tavernier, Geneviève, additional, Caspar-Bauguil, Sylvie, additional, Virtue, Sam, additional, Sramkova, Veronika, additional, Monbrun, Laurent, additional, Mazars, Anne, additional, Zanoun, Madjid, additional, Guilmeau, Sandra, additional, Barquissau, Valentin, additional, Beuzelin, Diane, additional, Bonnel, Sophie, additional, Marques, Marie, additional, Monge-Roffarello, Boris, additional, Lefort, Corinne, additional, Fielding, Barbara, additional, Sulpice, Thierry, additional, Astrup, Arne, additional, Payrastre, Bernard, additional, Bertrand-Michel, Justine, additional, Meugnier, Emmanuelle, additional, Ligat, Laetitia, additional, Lopez, Frédéric, additional, Guillou, Hervé, additional, Ling, Charlotte, additional, Holm, Cecilia, additional, Rabasa-Lhoret, Remi, additional, Saris, Wim H. M., additional, Stich, Vladimir, additional, Arner, Peter, additional, Rydén, Mikael, additional, Moro, Cedric, additional, Viguerie, Nathalie, additional, Harms, Matthew, additional, Hallén, Stefan, additional, Vidal-Puig, Antonio, additional, Vidal, Hubert, additional, Postic, Catherine, additional, and Langin, Dominique, additional

Published
2018
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29. Publisher Correction: Molecular phenomics and metagenomics of hepatic steatosis in non-diabetic obese women

Author

Hoyles, Lesley, primary, Fernández-Real, José-Manuel, additional, Federici, Massimo, additional, Serino, Matteo, additional, Abbott, James, additional, Charpentier, Julie, additional, Heymes, Christophe, additional, Luque, Jèssica Latorre, additional, Anthony, Elodie, additional, Barton, Richard H., additional, Chilloux, Julien, additional, Myridakis, Antonis, additional, Martinez-Gili, Laura, additional, Moreno-Navarrete, José Maria, additional, Benhamed, Fadila, additional, Azalbert, Vincent, additional, Blasco-Baque, Vincent, additional, Puig, Josep, additional, Xifra, Gemma, additional, Ricart, Wifredo, additional, Tomlinson, Christopher, additional, Woodbridge, Mark, additional, Cardellini, Marina, additional, Davato, Francesca, additional, Cardolini, Iris, additional, Porzio, Ottavia, additional, Gentileschi, Paolo, additional, Lopez, Frédéric, additional, Foufelle, Fabienne, additional, Butcher, Sarah A., additional, Holmes, Elaine, additional, Nicholson, Jeremy K., additional, Postic, Catherine, additional, Burcelin, Rémy, additional, and Dumas, Marc-Emmanuel, additional

Published
2018
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31. Liver Reptin/RUVBL2 controls glucose and lipid metabolism with opposite actions on mTORC1 and mTORC2 signalling

Author

Javary, Joaquim, primary, Allain-Courtois, Nathalie, additional, Saucisse, Nicolas, additional, Costet, Pierre, additional, Heraud, Capucine, additional, Benhamed, Fadila, additional, Pierre, Rémi, additional, Bure, Corinne, additional, Pallares-Lupon, Nestor, additional, Do Cruzeiro, Marcio, additional, Postic, Catherine, additional, Cota, Daniela, additional, Dubus, Pierre, additional, Rosenbaum, Jean, additional, and Benhamouche-Trouillet, Samira, additional

Published
2017
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32. Dietary oleic acid regulates hepatic lipogenesis through a liver X receptor-dependent signaling

Author

Ducheix, Simon, primary, Montagner, Alexandra, additional, Polizzi, Arnaud, additional, Lasserre, Frédéric, additional, Régnier, Marion, additional, Marmugi, Alice, additional, Benhamed, Fadila, additional, Bertrand-Michel, Justine, additional, Mselli-Lakhal, Laila, additional, Loiseau, Nicolas, additional, Martin, Pascal G., additional, Lobaccaro, Jean-Marc, additional, Ferrier, Laurent, additional, Postic, Catherine, additional, and Guillou, Hervé, additional

Published
2017
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33. L’hépatokine FGF21 est unique dans sa réponse nutrionnelle au glucose et au jeûne dans le foie : interdépendence des facteurs de transcription ChREBP et PPARα

Author

Iroz, Alison, primary, Montagner, Alexandra, additional, Benhamed, Fadila, additional, Polizzi, Arnaud, additional, Levavasseur, Françoise, additional, Antony, Elodie, additional, Régnier, Marion, additional, Fouché, Edwin, additional, Lukowicz, Céline, additional, Lippi, Yannick, additional, Daujat-Chavanieu, Martine, additional, Gerbal-Chalouin, Sabine, additional, Fauveau, Véronique, additional, Burnol, Anne-Françoise, additional, Walter Wahli, Sandra Guilmeau, additional, Dentin, Renaud, additional, Guillou, Hervé, additional, and Postic, Catherine, additional

Published
2017
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34. O-GlcNAcylation links ChREBP and FXR to glucose-sensing

Author

Benhamed, Fadila, Filhoulaud, Gaelle, Caron, Sandrine, Lefebvre, Philippe, Staels, Bart, Postic, Catherine, Institut Cochin (IC UM3 (UMR 8104 / U1016)), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Récepteurs nucléaires, maladies cardiovasculaires et diabète - U 1011 (RNMCD), Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), The work from the Institut Cochin INSERM U1016 was performed within the Département Hospitalo-Universitaire (DHU) AUToimmune and HORmonal diseaseS and supported by grants from the Agence Nationale de la Recherche (Crisalis, Genopath), Fondation Française de la Recherche Médicale (FRM, Labélisation Equipe) and the EU Grant FLORINASH (FP7). The work performed at Institut Pasteur INSERM UMR1011 was supported by grants from the EU Grant HEPADIP (no. 018734), the Region Nord-Pas-de-Calais/FEDER, the Agence Nationale de la Recherche (no. 11 BSV1 032 01), and European Genomic Institute for Diabetes (no. ANR-10-LABX-46). Bart Staels is a member of the Institut Universitaire de France., ANR-10-LABX-0046,EGID,EGID Diabetes Pole(2010), ANR-11-BSV1-0031,CRISALIS,Dialogue entre le signal insuline et le lipidome dans la stéatose(2011), ANR-13-BSV1-0009,EDD-GENOPATH,Les Pathologies Epileptogènes Développementales: approche intégrée pour améliorer le diagnostic et la compréhension des mécanismes physiopathologiques(2013), European Project: 241913,EC:FP7:HEALTH,FP7-HEALTH-2009-single-stage,FLORINASH(2010), European Project: 32591,HEPADIP, Centre National de la Recherche Scientifique (CNRS)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Cochin [IC UM3 (UMR 8104 / U1016)], Récepteurs nucléaires, maladies cardiovasculaires et diabète - U 1011 [RNMCD], Récepteurs nucléaires, lipoprotéines et athérosclérose, Bos, Mireille, EGID Diabetes Pole - - EGID2010 - ANR-10-LABX-0046 - LABX - VALID, BLANC - Dialogue entre le signal insuline et le lipidome dans la stéatose - - CRISALIS2011 - ANR-11-BSV1-0031 - BLANC - VALID, Blanc 2013 - Les Pathologies Epileptogènes Développementales: approche intégrée pour améliorer le diagnostic et la compréhension des mécanismes physiopathologiques - - EDD-GENOPATH2013 - ANR-13-BSV1-0009 - Blanc 2013 - VALID, The role of intestinal microflora in non-alcoholic fatty liver disease (NAFLD) - FLORINASH - - EC:FP7:HEALTH2010-01-01 - 2014-12-31 - 241913 - VALID, and Hepatic and adipose tissue and functions in the metabolic syndrome - HEPADIP - 32591 - OLD

Subjects
glucose-sensing, Endocrinology, O-GlcNAcylation, lcsh:RC648-665, FXR, ChREBP, Mini Review, [SDV.BBM] Life Sciences [q-bio]/Biochemistry, Molecular Biology, Liver metabolism, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, lcsh:Diseases of the endocrine glands. Clinical endocrinology
Abstract

Mini review article; International audience; Accumulating evidence suggests that O-GlcNAc transferase, an enzyme responsible for O-GlcNAc post-translational modification acts as a nutrient sensor that links glucose and the hexosamine biosynthetic pathway to the regulation of transcriptional factors involved in energy homeostasis. In liver, glucose signaling is mediated by carbohydrate response element-binding protein (ChREBP), which stimulates glycolytic and lipogenic gene expres-sion through its binding on a specific ChoRE DNA sequence. Modulation of ChREBP by O-GlcNAcylation increases its DNA binding affinity and its activity. ChREBP transcriptional activity also depends on the presence of several other co-factors and transcriptional fac-tors. Among them, the nuclear Farnesoid X Receptor (FXR), a key transcription factor of bile acid metabolism involved in the gut–liver axis homeostasis was recently shown to directly interact with ChREBP, acting as a repressor on the ChoRE of glycolytic genes. Interestingly, similarly to ChREBP, FXR is O-GlcNAcylated in response to glucose. This review discusses the importance of ChREBP and FXR modifications through O-GlcNAcylation in liver and how glucose can modify their mutual affinity and transcriptional activity.

Published
2015
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36. Liver Reptin/RUVBL2 controls glucose and lipid metabolism with opposite actions on mTORC1 and mTORC2 signalling.

Author

Javary, Joaquim, Allain-Courtois, Nathalie, Saucisse, Nicolas, Costet, Pierre, Heraud, Capucine, Benhamed, Fadila, Pierre, Rémi, Bure, Corinne, Pallares-Lupon, Nestor, Cruzeiro, Marcio Do, Postic, Catherine, Cota, Daniela, Dubus, Pierre, Rosenbaum, Jean, and Benhamouche-Trouillet, Samira

Subjects
LIPID metabolism, LIVER cancer, HOMEOSTASIS, METABOLIC syndrome, FATTY liver
Published
2018
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37. CO-77 - L’hépatokine FGF21 est unique dans sa réponse nutrionnelle au glucose et au jeûne dans le foie : interdépendence des facteurs de transcription ChREBP et PPARα

Author

Iroz, Alison, Montagner, Alexandra, Benhamed, Fadila, Polizzi, Arnaud, Levavasseur, Françoise, Antony, Elodie, Régnier, Marion, Fouché, Edwin, Lukowicz, Céline, Lippi, Yannick, Daujat-Chavanieu, Martine, Gerbal-Chalouin, Sabine, Fauveau, Véronique, Burnol, Anne-Françoise, Walter Wahli, Sandra Guilmeau, Dentin, Renaud, Guillou, Hervé, and Postic, Catherine

Published
2017
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40. Brain glucagon-like peptide-1 increases insulin secretion and muscle insulin resistance to favor hepatic glycogen storage

Author

C. Ronald Kahn, Fadilha Benhamed, Claude Knauf, Miguel A. Iglesias, Catherine Postic, Christophe Perrin, Rémy Burcelin, Jean Girard, Jean-François Tanti, Elodie Bernard, T Grémeaux, Daniel J. Drucker, Jean François Maury, Nathalie M. Delzenne, Patrice D. Cani, Institut des Maladies Métaboliques et Cardiovasculaires (I2MC), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM), BENHAMED, Fadila, and UCL - MD/FARM - Ecole de pharmacie

Subjects
Blood Glucose, Male, Osmosis, Time Factors, medicine.medical_treatment, [SDV]Life Sciences [q-bio], chemistry.chemical_compound, Glycogen Synthase Kinase 3, Mice, Phosphatidylinositol 3-Kinases, 0302 clinical medicine, Glucagon-Like Peptide 1, Insulin Secretion, 1-Phosphatidylinositol 3-Kinase, Glucose homeostasis, Insulin, Phosphorylation, ComputingMilieux_MISCELLANEOUS, Mice, Knockout, 0303 health sciences, Glycogen, biology, Basic Helix-Loop-Helix Leucine Zipper Transcription Factors, Reverse Transcriptase Polymerase Chain Reaction, Muscles, digestive, oral, and skin physiology, Brain, Nuclear Proteins, General Medicine, Glucagon-like peptide-1, Insulin oscillation, [SDV] Life Sciences [q-bio], Adipose Tissue, Liver, hormones, hormone substitutes, and hormone antagonists, medicine.medical_specialty, endocrine system, 030209 endocrinology & metabolism, 03 medical and health sciences, Insulin resistance, Diabetes mellitus, Internal medicine, Hyperinsulinism, medicine, Animals, RNA, Messenger, 030304 developmental biology, Glycogen Synthase Kinase 3 beta, Dose-Response Relationship, Drug, business.industry, Glucose Tolerance Test, medicine.disease, Peptide Fragments, Receptor, Insulin, Mice, Inbred C57BL, Insulin receptor, Endocrinology, Glucose, chemistry, Hyperglycemia, biology.protein, Glucose Clamp Technique, Commentary, Insulin Resistance, business, Transcription Factors
Abstract

Intestinal glucagon-like peptide-1 (GLP-1) is a hormone released into the hepatoportal circulation that stimulates pancreatic insulin secretion. GLP-1 also acts as a neuropeptide to control food intake and cardiovascular functions, but its neural role in glucose homeostasis is unknown. We show that brain GLP-1 controlled whole-body glucose fate during hyperglycemic conditions. In mice undergoing a hyperglycemic hyperinsulinemic clamp, icv administration of the specific GLP-1 receptor antagonist exendin 9-39 (Ex9) increased muscle glucose utilization and glycogen content. This effect did not require muscle insulin action, as it also occurred in muscle insulin receptor KO mice. Conversely, icv infusion of the GLP-1 receptor agonist exendin 4 (Ex4) reduced insulin-stimulated muscle glucose utilization. In hyperglycemia achieved by i.v. infusion of glucose, icv Ex4, but not Ex9, caused a 4-fold increase in insulin secretion and enhanced liver glycogen storage. However, when glucose was infused intragastrically, icv Ex9 infusion lowered insulin secretion and hepatic glycogen levels, whereas no effects of icv Ex4 were observed. In diabetic mice fed a high-fat diet, a 1-month chronic i.p. Ex9 treatment improved glucose tolerance and fasting glycemia. Our data show that during hyperglycemia, brain GLP-1 inhibited muscle glucose utilization and increased insulin secretion to favor hepatic glycogen stores, preparing efficiently for the next fasting state.

Published
2005
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42. Hepatic gene regulation by glucose and polyunsaturated fatty acids: A role for ChREBP

Author

Renaud Dentin, Jean Girard, Fadila Benhamed, Catherine Postic, Pierre-Damien Denechaud, Institut Cochin (IC UM3 (UMR 8104 / U1016)), Centre National de la Recherche Scientifique (CNRS)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Département de Physiologie, Université de Montréal (UdeM), [Institut Cochin] Département Endocrinologie, métabolisme, diabète (EMD) (EMD), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université de Paris (UP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université de Paris (UP), Institut Cochin (UMR_S567 / UMR 8104), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), BENHAMED, Fadila, and Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité)

Subjects
[SDV]Life Sciences [q-bio], Medicine (miscellaneous), Biology, Carbohydrate metabolism, Mice, 03 medical and health sciences, 0302 clinical medicine, Animals, Humans, Glycolysis, Carbohydrate-responsive element-binding protein, Glycogen synthase, ComputingMilieux_MISCELLANEOUS, 030304 developmental biology, chemistry.chemical_classification, Regulation of gene expression, 0303 health sciences, Nutrition and Dietetics, Basic Helix-Loop-Helix Leucine Zipper Transcription Factors, Nuclear Proteins, Lipid metabolism, [SDV] Life Sciences [q-bio], Glucose, Gene Expression Regulation, Liver, chemistry, Biochemistry, Lipogenesis, Fatty Acids, Unsaturated, biology.protein, 030217 neurology & neurosurgery, Transcription Factors, Polyunsaturated fatty acid
Abstract

The liver is a major site for carbohydrate metabolism (glycolysis and glycogen synthesis) and triglyceride synthesis (lipogenesis). In the last decade, increasing evidence has emerged to show that nutrients, in particular, glucose and fatty acids, are able to regulate hepatic gene expression in a transcriptional manner. Indeed, although insulin was long thought to be the major regulator of hepatic gene expression, it is now clear that glucose metabolism rather that glucose itself also contributes substantially to the coordinated regulation of carbohydrate and lipid homeostasis in liver. In fact, the recent discovery of the glucose-signaling transcription factor carbohydrate responsive element binding protein (ChREBP) shed some light on the molecular mechanisms by which glycolytic and lipogenic genes are reciprocally regulated by glucose and fatty acids in liver. Here, we will review some of the recent studies that have begun to elucidate the regulation and function of this key transcription factor in liver. Indeed, a better understanding of the mechanisms by which glucose and fatty acids control hepatic gene expression may provide novel insight into the development of new therapeutic strategies for a better management of diseases involving blood glucose and/or disorders of lipid metabolism.

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44. O-GlcNacylation Links TxNIP to Inflammasome Activation in Pancreatic β Cells.

Author

Filhoulaud G, Benhamed F, Pagesy P, Bonner C, Fardini Y, Ilias A, Movassat J, Burnol AF, Guilmeau S, Kerr-Conte J, Pattou F, Issad T, and Postic C

Abstract

Thioredoxin interacting protein (TxNIP), which strongly responds to glucose, has emerged as a central mediator of glucotoxicity in pancreatic β cells. TxNIP is a scaffold protein interacting with target proteins to inhibit or stimulate their activity. Recent studies reported that high glucose stimulates the interaction of TxNIP with the inflammasome protein NLRP3 (NLR family, pyrin domain containing 3) to increase interleukin-1 β (IL1β) secretion by pancreatic β cells. To better understand the regulation of TxNIP by glucose in pancreatic β cells, we investigated the implication of O-linked β-N-acetylglucosamine (O-GlcNAcylation) in regulating TxNIP at the posttranslational level. O-GlcNAcylation of proteins is controlled by two enzymes: the O-GlcNAc transferase (OGT), which transfers a monosaccharide to serine/threonine residues on target proteins, and the O-GlcNAcase (OGA), which removes it. Our study shows that TxNIP is subjected to O-GlcNAcylation in response to high glucose concentrations in β cell lines. Modification of the O-GlcNAcylation pathway through manipulation of OGT or OGA expression or activity significantly modulates TxNIP O-GlcNAcylation in INS1 832/13 cells. Interestingly, expression and O-GlcNAcylation of TxNIP appeared to be increased in islets of diabetic rodents. At the mechanistic level, the induction of the O-GlcNAcylation pathway in human and rat islets promotes inflammasome activation as evidenced by enhanced cleaved IL1β. Overexpression of OGT in HEK293 or INS1 832/13 cells stimulates TxNIP and NLRP3 interaction, while reducing TxNIP O-GlcNAcylation through OGA overexpression destabilizes this interaction. Altogether, our study reveals that O-GlcNAcylation represents an important regulatory mechanism for TxNIP activity in β cells.

Published
2019
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45. [The transcription factor ChREBP: a key modulator of insulin sensitivity?].

Author

Benhamed F, Poupeau A, and Postic C

Subjects
Acetylation, Acylation, Adipose Tissue drug effects, Animals, Fatty Acids biosynthesis, Glucose metabolism, Humans, Liver drug effects, Mice, Obesity physiopathology, Protein Isoforms, Basic Helix-Loop-Helix Leucine Zipper Transcription Factors physiology, Insulin Resistance physiology
Abstract

The transcription factor ChREBP, whose activity is induced by glucose metabolism, is a key player in the induction of genes of de novo fatty acid synthesis (lipogenesis) in response to glucose. Recent studies have shown that an active lipogenesis via ChREBP activation was associated with improved insulin sensitivity in adipose tissue and liver in mice. In particular, ChREBP, by limiting toxicity related to the accumulation of deleterious fatty acids, would be a major player of hepatic insulin sensitivity. The analysis of cohort of obese patients showed a positive correlation between ChREBP expression in the subcutaneous and visceral white adipose tissue and insulin sensitivity. More complex results were however obtained for ChREBP and hepatic insulin sensitivity. The identification of a novel ChREBP isoform, ChREBPβ, may provide a better understanding of the relationship between ChREBP, lipogenesis and insulin sensitivity in human liver., (© 2013 médecine/sciences – Inserm.)

Published
2013
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46. [The regulation of gene expression by glucose].

Author

Girard J, Dentin R, Benhamed F, Denechaud PD, and Postic C

Subjects
Glycolysis genetics, Humans, Lipids genetics, Lipids physiology, Signal Transduction, Transcription Factors physiology, Transcription, Genetic, Triglycerides physiology, Gene Expression Regulation physiology, Glucose physiology
Abstract

Glucose should not be considered uniquely as a cellular fuel but also as a signaling molecule involved in the regulation of genes encoding glycolytic and lipogenic enzymes and, as such, in storage of triglycerides. Transcriptional effects of glucose on glycolytic and lipogenic enzymes involve a specific transcription factor, ChREBP, whose characteristics and mechanism of activation are described. Finally, the possible implication of ChREBP in the physiopathology of obesity and type 2 diabetes are discussed.

Published
2007
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