30 results on '"Ducheix, Simon"'
Search Results
2. Deletion of Stearoyl-CoA Desaturase-1 From the Intestinal Epithelium Promotes Inflammation and Tumorigenesis, Reversed by Dietary Oleate
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Ducheix, Simon, Peres, Claudia, Härdfeldt, Jennifer, Frau, Carla, Mocciaro, Gabriele, Piccinin, Elena, Lobaccaro, Jean-Marc, De Santis, Stefania, Chieppa, Marcello, Bertrand-Michel, Justine, Plateroti, Michelina, Griffin, Julian L., Sabbà, Carlo, Ntambi, James M., and Moschetta, Antonio
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- 2018
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3. The protective role of liver X receptor (LXR) during fumonisin B1-induced hepatotoxicity
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Régnier, Marion, Polizzi, Arnaud, Lukowicz, Céline, Smati, Sarra, Lasserre, Frédéric, Lippi, Yannick, Naylies, Claire, Laffitte, Joelle, Bétoulières, Colette, Montagner, Alexandra, Ducheix, Simon, Gourbeyre, Pascal, Ellero-Simatos, Sandrine, Menard, Sandrine, Bertrand-Michel, Justine, Al Saati, Talal, Lobaccaro, Jean-Marc, Burger, Hester M., Gelderblom, Wentzel C., Guillou, Hervé, Oswald, Isabelle P., and Loiseau, Nicolas
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- 2019
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4. PGC-1β Induces Susceptibility To Acetaminophen-Driven Acute Liver Failure
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Piccinin, Elena, Ducheix, Simon, Peres, Claudia, Arconzo, Maria, Vegliante, Maria Carmela, Ferretta, Anna, Bellafante, Elena, Villani, Gaetano, and Moschetta, Antonio
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- 2019
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5. Lipidomic analysis of adipose-derived extracellular vesicles reveals specific EV lipid sorting informative of the obesity metabolic state
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Blandin, Alexia, Dugail, Isabelle, Hilairet, Grégory, Ponnaiah, Maharajah, Ghesquière, Valentine, Froger, Josy, Ducheix, Simon, Fizanne, Lionel, Boursier, Jérôme, Cariou, Bertrand, Lhomme, Marie, and Le Lay, Soazig
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- 2023
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6. Adverse effects of long-term exposure to bisphenol A during adulthood leading to hyperglycaemia and hypercholesterolemia in mice
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Marmugi, Alice, Lasserre, Frederic, Beuzelin, Diane, Ducheix, Simon, Huc, Laurence, Polizzi, Arnaud, Chetivaux, Maud, Pineau, Thierry, Martin, Pascal, Guillou, Hervé, and Mselli-Lakhal, Laila
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- 2014
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7. Hepatic peroxisome proliferator‐activated receptor γ coactivator 1β drives mitochondrial and anabolic signatures that contribute to hepatocellular carcinoma progression in mice
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Piccinin, Elena, Peres, Claudia, Bellafante, Elena, Ducheix, Simon, Pinto, Claudio, Villani, Gaetano, and Moschetta, Antonio
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- 2018
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8. Is hepatic lipogenesis fundamental for NAFLD/NASH? A focus on the nuclear receptor coactivator PGC-1β
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Ducheix, Simon, Vegliante, Maria Carmela, Villani, Gaetano, Napoli, Nicola, Sabbà, Carlo, and Moschetta, Antonio
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- 2016
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9. Activation of the Constitutive Androstane Receptor induces hepatic lipogenesis and regulates Pnpla3 gene expression in a LXR-independent way
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Marmugi, Alice, Lukowicz, Céline, Lasserre, Frederic, Montagner, Alexandra, Polizzi, Arnaud, Ducheix, Simon, Goron, Adeline, Gamet-Payrastre, Laurence, Gerbal-Chaloin, Sabine, Pascussi, Jean Marc, Moldes, Marthe, Pineau, Thierry, Guillou, Hervé, and Mselli-Lakhal, Laila
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- 2016
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10. Liver PPARα is crucial for whole-body fatty acid homeostasis and is protective against NAFLD
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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
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- 2016
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11. Effect of obesity and metabolic syndrome on plasma oxysterols and fatty acids in human
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Tremblay-Franco, Marie, Zerbinati, Chiara, Pacelli, Antonio, Palmaccio, Giuseppina, Lubrano, Carla, Ducheix, Simon, Guillou, Hervé, and Iuliano, Luigi
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- 2015
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12. Reduction in gut‐derived MUFAs via intestinal stearoyl‐CoA desaturase 1 deletion drives susceptibility to NAFLD and hepatocarcinoma.
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Ducheix, Simon, Piccinin, Elena, Peres, Claudia, Garcia‐Irigoyen, Oihane, Bertrand‐Michel, Justine, Fouache, Allan, Cariello, Marica, Lobaccaro, Jean‐Marc, Guillou, Hervé, Sabbà, Carlo, Ntambi, James M., and Moschetta, Antonio
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NON-alcoholic fatty liver disease ,INTESTINES ,WESTERN diet ,FATTY liver ,LIVER cancer - Abstract
Nonalcoholic fatty liver disease (NAFLD) is defined by a set of hepatic conditions ranging from steatosis to steatohepatitis (NASH), characterized by inflammation and fibrosis, eventually predisposing to hepatocellular carcinoma (HCC). Together with fatty acids (FAs) originated from adipose lipolysis and hepatic lipogenesis, intestinal‐derived FAs are major contributors of steatosis. However, the role of mono‐unsaturated FAs (MUFAs) in NAFLD development is still debated. We previously established the intestinal capacity to produce MUFAs, but its consequences in hepatic functions are still unknown. Here, we aimed to determine the role of the intestinal MUFA‐synthetizing enzyme stearoyl‐CoA desaturase 1 (SCD1) in NAFLD. We used intestinal‐specific Scd1‐KO (iScd1−/−) mice and studied hepatic dysfunction in different models of steatosis, NASH, and HCC. Intestinal‐specific Scd1 deletion decreased hepatic MUFA proportion. Compared with controls, iScd1−/− mice displayed increased hepatic triglyceride accumulation and derangement in cholesterol homeostasis when fed a MUFA‐deprived diet. Then, on Western diet feeding, iScd1−/− mice triggered inflammation and fibrosis compared with their wild‐type littermates. Finally, intestinal‐Scd1 deletion predisposed mice to liver cancer. Conclusions: Collectively, these results highlight the major importance of intestinal MUFA metabolism in maintaining hepatic functions and show that gut‐derived MUFAs are protective from NASH and HCC. [ABSTRACT FROM AUTHOR]
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- 2022
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13. The liver X receptor: A master regulator of the gut–liver axis and a target for non alcoholic fatty liver disease
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Ducheix, Simon, Montagner, Alexandra, Theodorou, Vassilia, Ferrier, Laurent, and Guillou, Hervé
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- 2013
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14. Low Doses of Bisphenol A Induce Gene Expression Related to Lipid Synthesis and Trigger Triglyceride Accumulation in Adult Mouse Liver
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Marmugi, Alice, Ducheix, Simon, Lasserre, Frédéric, Polizzi, Arnaud, Paris, Alain, Priymenko, Nathalie, Bertrand-Michel, Justine, Pineau, Thierry, Guillou, Hervé, Martin, Pascal G.P., and Mselli-Lakhal, Laïla
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- 2012
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15. LXRs, SHP, and FXR in Prostate Cancer: Enemies or Ménage à Quatre With AR?
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Baron, Silvère, Cariello, Marica, DUCHEIX, Simon, Maqdasy, Salwan, Baron, Silvere, Moschetta, Antonio, Lobaccaro, Jean-Marc, Génétique, Reproduction et Développement - Clermont Auvergne (GReD), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Clermont Auvergne (UCA)-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), Department of Translational Pharmacology, Génétique, Reproduction et Développement (GReD), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Clermont Auvergne [2017-2020] (UCA [2017-2020])-Centre National de la Recherche Scientifique (CNRS), Institut National de la Recherche Agronomique (INRA)-Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT)-Université de Toulouse (UT)-Ecole Nationale Vétérinaire de Toulouse (ENVT), Université de Toulouse (UT)-Université de Toulouse (UT)-Institut National Polytechnique (Toulouse) (Toulouse INP), Université de Toulouse (UT)-Ecole d'Ingénieurs de Purpan (INP - PURPAN), Université de Toulouse (UT)-Université de Toulouse (UT), and Centre National de la Recherche Scientifique (CNRS)-Université Clermont Auvergne [2017-2020] (UCA [2017-2020])-Institut National de la Santé et de la Recherche Médicale (INSERM)
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0301 basic medicine ,medicine.drug_class ,[SDV]Life Sciences [q-bio] ,General Medicine ,Biology ,Androgen ,medicine.disease ,3. Good health ,Androgen receptor ,03 medical and health sciences ,Prostate cancer ,030104 developmental biology ,0302 clinical medicine ,Nuclear receptor ,030220 oncology & carcinogenesis ,medicine ,Cancer research ,Small heterodimer partner ,Farnesoid X receptor ,Liver X receptor ,Receptor ,ComputingMilieux_MISCELLANEOUS - Abstract
Androgens and androgen receptor (AR, NR3C4) clearly play a crucial role in prostate cancer progression. Besides, the link between metabolic disorders and the risk of developing a prostate cancer has been emerging these last years. Interestingly, “lipid” nuclear receptors such as LXRα/NR1H3 and LXRβ/NR1H2 (as well as FXRα/NR1H4 and SHP/NR0B2) have been described to decrease the lipid metabolism, while AR increases it. Moreover, these former orphan nuclear receptors can regulate androgen levels and modulate AR activity. Thus, it is not surprising to find such receptors involved in the physiology of prostate. This review is focused on the roles of liver X receptors (LXRs), farnesoid X receptor (FXR), and small heterodimeric partner (SHP) in prostate physiology and their capabilities to interfere with the androgen-regulated pathways by modulating the levels of active androgen within the prostate. By the use of prostate cancer cell lines, mice deficient for these nuclear receptors and human tissue libraries, several authors have pointed out the putative possibility to pharmacologically target these receptors. These data open a new field of research for the development of new drugs that could overcome the castration resistance in prostate cancer, a usual phenomenon in patients.
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- 2018
16. Chronic O-GlcNAcylation and Diabetic Cardiomyopathy: The Bitterness of Glucose
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Ducheix, Simon, Magré, Jocelyne, Cariou, Bertrand, and Prieur, Xavier
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Endocrinology ,glucotoxicity ,O-GlcNAcylation ,lcsh:RC648-665 ,diabetes ,Review ,metabolism ,cardiomyopathy ,lcsh:Diseases of the endocrine glands. Clinical endocrinology - Abstract
Type 2 diabetes (T2D) is a major risk factor for heart failure. Diabetic cardiomyopathy (DC) is characterized by diastolic dysfunction and left ventricular hypertrophy. Epidemiological data suggest that hyperglycaemia contributes to the development of DC. Several cellular pathways have been implicated in the deleterious effects of high glucose concentrations in the heart: oxidative stress, accumulation of advanced glycation end products (AGE), and chronic hexosamine biosynthetic pathway (HBP) activation. In the present review, we focus on the effect of chronic activation of the HBP on diabetic heart function. The HBP supplies N-acetylglucosamine moiety (O-GlcNAc) that is O-linked by O-GlcNAc transferase (OGT) to proteins on serine or threonine residues. This post-translational protein modification modulates the activity of the targeted proteins. In the heart, acute activation of the HBP in response to ischaemia-reperfusion injury appears to be protective. Conversely, chronic activation of the HBP in the diabetic heart affects Ca2+ handling, contractile properties, and mitochondrial function and promotes stress signaling, such as left ventricular hypertrophy and endoplasmic reticulum stress. Many studies have shown that O-GlcNAc impairs the function of key protein targets involved in these pathways, such as phospholamban, calmodulin kinase II, troponin I, and FOXO1. The data show that excessive O-GlcNAcylation is a major trigger of the glucotoxic events that affect heart function under chronic hyperglycaemia. Supporting this finding, pharmacological or genetic inhibition of the HBP in the diabetic heart improves heart function. In addition, the SGLT2 inhibitor dapagliflozin, a glucose lowering agent, has recently been shown to lower cardiac HBP in a lipodystophic T2D mice model and to concomitantly improve the diastolic dysfunction of these mice. Therefore, targeting cardiac-excessive O-GlcNAcylation or specific target proteins represents a potential therapeutic option to treat glucotoxicity in the diabetic heart.
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- 2018
17. Protective effects of n-6 fatty acids-enriched diet on intestinal ischaemia/reperfusion injury involve lipoxin A4 and its receptor
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Gobbetti, Thomas, DUCHEIX, Simon, Le Faouder, Pauline, Pérez-Berezo, Teresa, Riols, Fabien, Boué, Jérôme, Bertrand-Michel, Justine, Dubourdeau, Marc, Guillou, Hervé, Perretti, Mauro, Vergnolle, Nathalie, Cenac, Nicolas, Centre de Physiopathologie Toulouse Purpan ex IFR 30 et IFR 150 (CPTP), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS), Centre National de la Recherche Scientifique (CNRS), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées, WHRI, Queen Mary University of London (QMUL), ToxAlim (ToxAlim), 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), Lipidomic Core Facility, Plateforme MetaToul, Institut des Maladies Métaboliques et Cardiovasculaires (I2MC), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM), Ambiotis (Ambiotis), This work was supported by the Agence Nationale de la Recherche (to N. V., ANR-12-BSV1-0030-01 and N. C., ANR-12-JSV1-0001-01), the INSERM (to N. V.), two grants from the Region Midi-Pyrenees (to P. L. F. and N. C.), the European Research Council (to N. V., ERC-2012-StG-20111109) and the Wellcome Trust (program 086867/Z/08/Z, to T. G. and M. P.), Centre de Physiopathologie Toulouse Purpan (CPTP), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Plateau MetaToul-LIPIDOMIQUE = MetaToul-Lipidomics, Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-MetaToul-MetaboHUB, Génopole Toulouse Midi-Pyrénées [Auzeville] (GENOTOUL), Institut National des Sciences Appliquées - Toulouse (INSA Toulouse), Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Ecole Nationale Vétérinaire de Toulouse (ENVT), Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE)-Institut National des Sciences Appliquées - Toulouse (INSA Toulouse), Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE)-Génopole Toulouse Midi-Pyrénées [Auzeville] (GENOTOUL), Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Ecole Nationale Vétérinaire de Toulouse (ENVT), Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées, 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 National de la Recherche Agronomique (INRA)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Ecole d'Ingénieurs de Purpan (INPT - EI Purpan), ProdInra, Archive Ouverte, Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-MetaboHUB-MetaToul, Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE)-Ecole Nationale Vétérinaire de Toulouse (ENVT), and Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-MetaToul-MetaboHUB
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Male ,appareil intestinal ,[SDV]Life Sciences [q-bio] ,acide gras polyinsaturé n 6 ,maladie intestinale ,Mice ,Structure-Activity Relationship ,ischémie reperfusion ,Ischemia ,acide gras polyinsaturé ,Fatty Acids, Omega-6 ,Animals ,Intestinal Mucosa ,intussusception ,acide gras ,polyunsaturated fatty acid ,reperfusion injury ,Research Papers ,Receptors, Formyl Peptide ,Diet ,Intestines ,Lipoxins ,Mice, Inbred C57BL ,[SDV] Life Sciences [q-bio] ,régime alimentaire ,acide gras polyinsaturé n-3 ,fatty acid - Abstract
Long-term intake of dietary fatty acids is known to predispose to chronic inflammation, but their effects on acute intestinal ischaemia/reperfusion (I/R) injury is unknown. The aim of this study was to determine the consequences of a diet rich in n-3 or n-6 polyunsaturated fatty acids (PUFA) on intestinal I/R-induced damage. Mice were fed three different isocaloric diets: a balanced diet used as a control and two different PUFA-enriched diets, providing either high levels of n-3 or of n-6 PUFA. Intestinal injury was evaluated after intestinal I/R. PUFA metabolites were quantitated in intestinal tissues by LC-MS/MS. In control diet-fed mice, intestinal I/R caused inflammation and increased COX and lipoxygenase-derived metabolites compared with sham-operated animals. Lipoxin A4 (LxA4 ) was significantly and selectively increased after ischaemia. Animals fed a high n-3 diet did not display a different inflammatory profile following intestinal I/R compared with control diet-fed animals. In contrast, intestinal inflammation was decreased in the I/R group fed with high n-6 diet and level of LxA4 was increased post-ischaemia compared with control diet-fed mice. Blockade of the LxA4 receptor (Fpr2), prevented the anti-inflammatory effects associated with the n-6 rich diet. This study indicates that high levels of dietary n-6, but not n-3, PUFAs provides significant protection against intestinal I/R-induced damage and demonstrates that the endogenous production of LxA4 can be influenced by diet.
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- 2015
18. Role of LXR in the regulation of hepatic lipogenesis in response to dietary fatty acids
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Ducheix, Simon, Montagner, Alexandra, Podechard, Normand, Bertrand-Michel, J., Polizzi, Arnaud, Lobaccaro, Jean-Marc, Pineau, Thierry, Martin, Pascal G.P., Guillou, Hervé, 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), and ProdInra, Migration
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[SDV] Life Sciences [q-bio] ,[SDV]Life Sciences [q-bio] ,ComputingMilieux_MISCELLANEOUS - Abstract
International audience
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- 2011
19. Extract RNAs but keep the lipids: a useful trick in the field of nuclear receptors biology
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Polizzi, Arnaud, Podechard, Normand, Ducheix, Simon, Bertrand-Michel, J., Lasserre, Frédéric, Loiseau, Nicolas, Lobaccaro, Jean-Marc, Pineau, Thierry, Martin, Pascal G.P., Guillou, Hervé, Toxicologie Intégrative & Métabolisme (ToxAlim-TIM), 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)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Recherche Agronomique (INRA), and ProdInra, Migration
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[SDV] Life Sciences [q-bio] ,[SDV]Life Sciences [q-bio] ,ComputingMilieux_MISCELLANEOUS - Abstract
International audience
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- 2011
20. Dietary oleic acid regulates hepatic lipogenesis through a liver X receptor-dependent signaling.
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Ducheix, Simon, Montagner, Alexandra, Polizzi, Arnaud, Lasserre, Frédéric, Régnier, Marion, Marmugi, Alice, Benhamed, Fadila, Bertrand-Michel, Justine, Mselli-Lakhal, Laila, Loiseau, Nicolas, Martin, Pascal G., Lobaccaro, Jean-Marc, Ferrier, Laurent, Postic, Catherine, and Guillou, Hervé
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OLEIC acid , *DIETARY supplements , *LIPID synthesis , *CELL communication , *LIVER physiology , *CARDIOVASCULAR diseases - Abstract
Olive oil consumption is beneficial for health as it is associated with a decreased prevalence of cancer and cardiovascular diseases. Oleic acid is, by far, the most abundant component of olive oil. Since it can be made through de novo synthesis in animals, it is not an essential fatty acid. While it has become clear that dietary oleic acid regulates many biological processes, the signaling pathway involved in these regulations remains poorly defined. In this work we tested the impact of an oleic acid-rich diet on hepatic gene expression. We were particularly interested in addressing the contribution of Liver X Receptors (LXR) in the control of genes involved in hepatic lipogenesis, an essential process in whole body energy homeostasis. We used wild-type mice and transgenic mice deficient for both α and β Liver X Receptor isoforms (LXR-/-) fed a control or an oleate enriched diet. We observed that hepatic-lipid accumulation was enhanced as well as the expression of lipogenic genes in the liver of wild-type mice fed the oleate enriched diet. In contrast, none of these changes occurred in the liver of LXR-/- mice. Strikingly, oleate-rich diet reduced cholesterolemia in wild-type mice and induced signs of liver inflammation and damage in LXR-/- mice but not in wild-type mice. This work suggests that dietary oleic acid reduces cholesterolemia while promoting LXR-dependent hepatic lipogenesis without detrimental effects to the liver. [ABSTRACT FROM AUTHOR]
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- 2017
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21. Hepatic Fasting-Induced PPARα Activity Does Not Depend on Essential Fatty Acids.
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Polizzi, Arnaud, Fouché, Edwin, Ducheix, Simon, Lasserre, Frédéric, Marmugi, Alice P., Mselli-Lakhal, Laila, Loiseau, Nicolas, Wahli, Walter, Guillou, Hervé, and Montagner, Alexandra
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PEROXISOME proliferator-activated receptors ,ESSENTIAL fatty acids ,NUCLEAR receptors (Biochemistry) ,FASTING ,LIGANDS (Biochemistry) - Abstract
The liver plays a central role in the regulation of fatty acid metabolism, which is highly sensitive to transcriptional responses to nutrients and hormones. Transcription factors involved in this process include nuclear hormone receptors. One such receptor, PPARα, which is highly expressed in the liver and activated by a variety of fatty acids, is a critical regulator of hepatic fatty acid catabolism during fasting. The present study compared the influence of dietary fatty acids and fasting on hepatic PPARα-dependent responses. Pparaα
-/- male mice and their wild-type controls were fed diets containing different fatty acids for 10 weeks prior to being subjected to fasting or normal feeding. In line with the role of PPARα in sensing dietary fatty acids, changes in chronic dietary fat consumption influenced liver damage during fasting. The changes were particularly marked in mice fed diets lacking essential fatty acids. However, fasting, rather than specific dietary fatty acids, induced acute PPARα activity in the liver. Taken together, the data imply that the potent signalling involved in triggering PPARα activity during fasting does not rely on essential fatty acid-derived ligand. [ABSTRACT FROM AUTHOR]- Published
- 2016
- Full Text
- View/download PDF
22. Essential fatty acids deficiency promotes lipogenic gene expression and hepatic steatosis through the liver X receptor
- Author
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Ducheix, Simon, Montagner, Alexandra, Polizzi, Arnaud, Lasserre, Frédéric, Marmugi, Alice, Bertrand-Michel, Justine, Podechard, Normand, Al Saati, Talal, Chétiveaux, Maud, Baron, Silvère, Boué, Jérôme, Dietrich, Gilles, Mselli-Lakhal, Laila, Costet, Philippe, Lobaccaro, Jean-Marc A., Pineau, Thierry, Theodorou, Vassilia, Postic, Catherine, Martin, Pascal G.P., and Guillou, Hervé
- Subjects
- *
FATTY acid deficiency , *FATTY liver , *GENE expression , *FATTY degeneration , *LIPID synthesis , *ESSENTIAL fatty acids , *EICOSAPENTAENOIC acid - Abstract
Background & Aims: Nutrients influence non-alcoholic fatty liver disease. Essential fatty acids deficiency promotes various syndromes, including hepatic steatosis, through increased de novo lipogenesis. The mechanisms underlying such increased lipogenic response remain unidentified. Methods: We used wild type mice and mice lacking Liver X Receptors to perform a nutrigenomic study that aimed at examining the role of these transcription factors. Results: We showed that, in the absence of Liver X Receptors, essential fatty acids deficiency does not promote steatosis. Consistent with this, Liver X Receptors are required for the elevated expression of genes involved in lipogenesis in response to essential fatty acids deficiency. Conclusions: This work identifies, for the first time, the central role of Liver X Receptors in steatosis induced by essential fatty acids deficiency. [Copyright &y& Elsevier]
- Published
- 2013
- Full Text
- View/download PDF
23. A systems biology approach to the hepatic role of the oxysterol receptor LXR in the regulation of lipogenesis highlights a cross-talk with PPARα
- Author
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Ducheix, Simon, Podechard, Normand, Lasserre, Frédéric, Polizzi, Arnaud, Pommier, Aurélien, Murzilli, Stefania, Di Lisio, Chiara, D’Amore, Simona, Bertrand-Michel, Justine, Montagner, Alexandra, Pineau, Thierry, Loiseau, Nicolas, Lobaccaro, Jean-Marc, Martin, Pascal G.P., and Guillou, Hervé
- Subjects
- *
SYSTEMS biology , *LIPID synthesis , *OXYSTEROLS , *PEROXISOME proliferator-activated receptors , *TRANSCRIPTION factors , *NUCLEAR receptors (Biochemistry) , *LIVER - Abstract
Abstract: The Liver X Receptors (LXRs) α and β and the Peroxisome Proliferator-Activated Receptor α (PPARα) are transcription factors that belong to class II nuclear receptors. They drive the expression of genes involved in hepatic lipid homeostasis and therefore are important targets for the prevention and treatment of nonalcoholic fatty liver disease (NAFLD). LXRs and PPARα are regulated by endogenous ligands, oxysterols and fatty acid derived molecules, respectively. In the liver, pharmacological activation of LXRs leads to the over-expression of genes involved in de novo lipogenesis, while PPARα is critical for fatty acid catabolism in nutrient deprivation. Even if these two nuclear receptors seemed to play opposite parts, recent studies have highlighted that PPARα also influence the expression of genes involved in fatty acids synthesis. In this study, we used pharmacological approaches and genetically engineered mice to investigate the cross-talk between LXRs and PPARα in the regulation of genes responsible for lipogenesis. We first investigated the effect of T0901317 and fenofibrate, two synthetic agonists of LXRs and PPARα, respectively. As expected, T0901317 and fenofibrate induce expression of genes involved LXR-dependent and PPARα-dependent lipogenic responses. Considering such overlapping effect, we then tested whether LXR agonist may influence PPARα driven response and vice versa. We show that the lack of PPARα does not influence the effects of T0901317 on lipogenic genes expression. However, PPARα deficiency prevents the up-regulation of genes involved in ω-hydroxylation that are induced by the LXR agonist. In addition, over-expression of lipogenic genes in response to fenofibrate is decreased in LXR knockout mice as well as the expression of PPARα target genes involved in fatty acid oxidation. Altogether, our work provides in vivo evidence for a central interconnection between nuclear receptors that drive hepatic lipid metabolism in response to oxysterol and fatty acids. [Copyright &y& Elsevier]
- Published
- 2013
- Full Text
- View/download PDF
24. Seipin localizes at endoplasmic-reticulum-mitochondria contact sites to control mitochondrial calcium import and metabolism in adipocytes.
- Author
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Combot, Yoann, Salo, Veijo T., Chadeuf, Gilliane, Hölttä, Maarit, Ven, Katharina, Pulli, Ilari, Ducheix, Simon, Pecqueur, Claire, Renoult, Ophélie, Lak, Behnam, Li, Shiqian, Karhinen, Leena, Belevich, Ilya, Le May, Cedric, Rieusset, Jennifer, Le Lay, Soazig, Croyal, Mikael, Tayeb, Karim Si, Vihinen, Helena, and Jokitalo, Eija
- Abstract
Deficiency of the endoplasmic reticulum (ER) protein seipin results in generalized lipodystrophy by incompletely understood mechanisms. Here, we report mitochondrial abnormalities in seipin-deficient patient cells. A subset of seipin is enriched at ER-mitochondria contact sites (MAMs) in human and mouse cells and localizes in the vicinity of calcium regulators SERCA2, IP3R, and VDAC. Seipin association with MAM calcium regulators is stimulated by fasting-like stimuli, while seipin association with lipid droplets is promoted by lipid loading. Acute seipin removal does not alter ER calcium stores but leads to defective mitochondrial calcium import accompanied by a widespread reduction in Krebs cycle metabolites and ATP levels. In mice, inducible seipin deletion leads to mitochondrial dysfunctions preceding the development of metabolic complications. Together, these data suggest that seipin controls mitochondrial energy metabolism by regulating mitochondrial calcium influx at MAMs. In seipin-deficient adipose tissue, reduced ATP production compromises adipocyte properties, contributing to lipodystrophy pathogenesis. [Display omitted] • Seipin is enriched at ER-MAMs • Seipin interacts with MAM calcium regulators in a nutritionally regulated manner • Adipocyte seipin deficiency impairs mitochondrial calcium import and ATP production • Inducible seipin removal from adipose tissue leads to rapid mitochondrial dysfunction Combot et al. demonstrate that seipin is enriched at ER-mitochondria contact sites and that seipin deficiency leads to defective mitochondrial calcium import accompanied by a reduction in ATP production. In mice, inducible seipin deletion from adipocytes leads to early mitochondrial dysfunction, which probably contributes to the pathogenesis of seipin-related lipodystrophy. [ABSTRACT FROM AUTHOR]
- Published
- 2022
- Full Text
- View/download PDF
25. Proton NMR Enables the Absolute Quantification of Aqueous Metabolites and Lipid Classes in Unique Mouse Liver Samples.
- Author
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Amiel, Aurélien, Tremblay-Franco, Marie, Gautier, Roselyne, Ducheix, Simon, Montagner, Alexandra, Polizzi, Arnaud, Debrauwer, Laurent, Guillou, Hervé, Bertrand-Michel, Justine, and Canlet, Cécile
- Subjects
SATURATED fatty acids ,LACTATES ,PROTON magnetic resonance ,MONOUNSATURATED fatty acids ,NUCLEAR magnetic resonance ,ORGANIC solvents ,HYDROXYCHOLESTEROLS ,LIPIDS - Abstract
Hepatic metabolites provide valuable information on the physiological state of an organism, and thus, they are monitored in many clinical situations. Typically, monitoring requires several analyses for each class of targeted metabolite, which is time consuming. The present study aimed to evaluate a proton nuclear magnetic resonance (
1 H-NMR) method for obtaining quantitative measurements of aqueous and lipidic metabolites. We optimized the extraction protocol, the standard samples, and the organic solvents for the absolute quantification of lipid species. To validate the method, we analyzed metabolic profiles in livers of mice fed three different diets. We compared our results with values obtained with conventional methods and found strong correlations. The1 H-NMR protocol enabled the absolute quantification of 29 aqueous metabolites and eight lipid classes. Results showed that mice fed a diet enriched in saturated fatty acids had higher levels of triglycerides, cholesterol ester, monounsaturated fatty acids, lactate, 3-hydroxy-butyrate, and alanine and lower levels of glucose, compared to mice fed a control diet. In conclusion, proton NMR provided a rapid overview of the main lipid classes (triglycerides, cholesterol, phospholipids, fatty acids) and the most abundant aqueous metabolites in liver. [ABSTRACT FROM AUTHOR]- Published
- 2020
- Full Text
- View/download PDF
26. Role of Oleic Acid in the Gut-Liver Axis: From Diet to the Regulation of Its Synthesis via Stearoyl-CoA Desaturase 1 (SCD1).
- Author
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Piccinin, Elena, Cariello, Marica, De Santis, Stefania, Ducheix, Simon, Sabbà, Carlo, Ntambi, James M., and Moschetta, Antonio
- Abstract
The consumption of an olive oil rich diet has been associated with the diminished incidence of cardiovascular disease and cancer. Several studies have attributed these beneficial effects to oleic acid (C18 n-9), the predominant fatty acid principal component of olive oil. Oleic acid is not an essential fatty acid since it can be endogenously synthesized in humans. Stearoyl-CoA desaturase 1 (SCD1) is the enzyme responsible for oleic acid production and, more generally, for the synthesis of monounsaturated fatty acids (MUFA). The saturated to monounsaturated fatty acid ratio affects the regulation of cell growth and differentiation, and alteration in this ratio has been implicated in a variety of diseases, such as liver dysfunction and intestinal inflammation. In this review, we discuss our current understanding of the impact of gene-nutrient interactions in liver and gut diseases, by taking advantage of the role of SCD1 and its product oleic acid in the modulation of different hepatic and intestinal metabolic pathways. [ABSTRACT FROM AUTHOR]
- Published
- 2019
- Full Text
- View/download PDF
27. LXRs, SHP, and FXR in Prostate Cancer: Enemies or Ménage à Quatre With AR?
- Author
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Cariello, Marica, Ducheix, Simon, Maqdasy, Salwan, Baron, Silvère, Moschetta, Antonio, and Lobaccaro, Jean-Marc A.
- Published
- 2018
- Full Text
- View/download PDF
28. Key role of the ERK1/2 MAPK pathway in the transcriptional regulation of the Stearoyl-CoA Desaturase (SCD1) gene expression in response to leptin
- Author
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Mauvoisin, Daniel, Prévost, Michèle, Ducheix, Simon, Arnaud, Marie-Pierre, and Mounier, Catherine
- Subjects
- *
MITOGEN-activated protein kinases , *GENETIC transcription regulation , *GENE expression , *LEPTIN , *TRANSCRIPTION factors , *FATTY acid synthesis , *CELLULAR signal transduction , *CHEMICAL inhibitors - Abstract
Abstract: Stearoyl-CoA Desaturase-1 (SCD1) is the rate limiting enzyme catalyzing the synthesis of monounsaturated fatty acids. Variation of SCD1 activity and the ratio of saturated to unsaturated fatty acids have been implicated in a variety of diseases including obesity, type II diabetes and cancers. In liver, many factors regulate SCD1 expression including dietary and hormonal factors such as insulin and leptin. We previously showed in hepatic cells that insulin acts through the PI3K and mTOR pathways to upregulate SCD1 expression. In the present study, using HepG2 cells, we characterized the signaling pathway mediating the leptin inhibitory response on SCD1 gene expression. We showed that leptin inhibits SCD1 at the transcriptional level. Inhibition of the ERK1/2 MAPK pathway with the PD98059 reverses the effect of leptin on SCD1 expression. Our data also demonstrated that the effect of leptin is entirely independent of the effect of insulin. Using the pharmaceutical inhibitors Ag490 and SL0101, we showed that the inhibitory effect of leptin is also mediated by the Janus Kinase 2 (Jak2) and p90RSK. EMSA and transfection experiments suggest a key role for the Sp1 transcription factor, which in turn may compete for the binding of other transcription factors such as AP-1, leading to the inhibition of SCD1 transcription. Taken together, our observations showed that, independently of insulin action, leptin exerts an inhibitory effect on SCD1 transcription via a signaling pathway implicating Jak2, ERK1/2, and p90RSK which probably targets the downstream transcription factor Sp1 on the SCD1 promoter. [Copyright &y& Elsevier]
- Published
- 2010
- Full Text
- View/download PDF
29. Proton NMR Enables the Absolute Quantification of Aqueous Metabolites and Lipid Classes in Unique Mouse Liver Samples.
- Author
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Amiel A, Tremblay-Franco M, Gautier R, Ducheix S, Montagner A, Polizzi A, Debrauwer L, Guillou H, Bertrand-Michel J, and Canlet C
- Abstract
Hepatic metabolites provide valuable information on the physiological state of an organism, and thus, they are monitored in many clinical situations. Typically, monitoring requires several analyses for each class of targeted metabolite, which is time consuming. The present study aimed to evaluate a proton nuclear magnetic resonance (
1 H-NMR) method for obtaining quantitative measurements of aqueous and lipidic metabolites. We optimized the extraction protocol, the standard samples, and the organic solvents for the absolute quantification of lipid species. To validate the method, we analyzed metabolic profiles in livers of mice fed three different diets. We compared our results with values obtained with conventional methods and found strong correlations. The1 H-NMR protocol enabled the absolute quantification of 29 aqueous metabolites and eight lipid classes. Results showed that mice fed a diet enriched in saturated fatty acids had higher levels of triglycerides, cholesterol ester, monounsaturated fatty acids, lactate, 3-hydroxy-butyrate, and alanine and lower levels of glucose, compared to mice fed a control diet. In conclusion, proton NMR provided a rapid overview of the main lipid classes (triglycerides, cholesterol, phospholipids, fatty acids) and the most abundant aqueous metabolites in liver.- Published
- 2019
- Full Text
- View/download PDF
30. Dual extraction of mRNA and lipids from a single biological sample.
- Author
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Podechard N, Ducheix S, Polizzi A, Lasserre F, Montagner A, Legagneux V, Fouché E, Saez F, Lobaccaro JM, Lakhal L, Ellero-Simatos S, Martin PG, Loiseau N, Bertrand-Michel J, and Guillou H
- Subjects
- Animals, Chemical Fractionation methods, Gene Expression Profiling, Lipids chemistry, Liver chemistry, Liver metabolism, Mice, RNA, Messenger chemistry, Reproducibility of Results, Lipids isolation & purification, RNA, Messenger isolation & purification
- Abstract
The extraction of RNA and lipids from a large number of biological samples is time-consuming and costly with steps required for both transcriptomic and lipidomic approaches. Most protocols rely on independent extraction of nucleic acids and lipids from a single sample, thereby increasing the need for biological material and inducing variability in data analysis. We investigated whether it is possible to use a standard RNA extraction procedure to analyze not only RNA levels, but also lipids in a single liver sample. We show that the organic phase obtained when using standard reagents for RNA extraction can be used to analyze lipids, including neutral lipids and fatty acids, by gas chromatography. We applied this technique to an analysis of lipids and the associated gene expression pattern in mice with hepatic steatosis induced by pharmacological activation of nuclear receptor LXR.
- Published
- 2018
- Full Text
- View/download PDF
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