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2. Good outcome of liver transplantation in patients with pre-existing renal cell carcinoma

Author

Lassailly, G., primary, Ningarhari, M., additional, Dumortier, J, additional, Lafforgue, C., additional, Bouye, S., additional, Amrani, M.El, additional, Lebuffe, G., additional, Villers, A., additional, Truant, S, additional, Mathurin, P., additional, Louvet, A., additional, Boillot, O, additional, Boleslawski, E, additional, and Dharancy, S., additional

Published
2023
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6. 1854P Multicentric, comparative, retrospective study on the safety and efficacy of conventional chemotherapy in cirrhotic patients with gastrointestinal cancer

Author

Ningarhari, M., primary, Bertez, M., additional, Ploquin, A., additional, Bertrand, N., additional, Desauw, C., additional, Cattan, S., additional, Catala, P., additional, Vandamme, H., additional, Wasselin, J., additional, Lubret, H., additional, Cheymol, C., additional, Truant, S., additional, Lassailly, G., additional, Canva, V., additional, Louvet, A., additional, Mathurin, P., additional, Dharancy, S., additional, and Turpin, A., additional

Published
2021
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8. Increased Hepatic PDGF-AA Signaling Mediates Liver Insulin Resistance in Obesity-Associated Type 2 Diabetes

Author

Abderrahmani, A, Yengo, L, Caiazzo, R, Canouil, M, Cauchi, S, Raverdy, V, Plaisance, V, Pawlowski, V, Lobbens, S, Maillet, J, Rolland, L, Boutry, R, Queniat, G, Kwapich, M, Tenenbaum, M, Bricambert, J, Saussenthaler, S, Anthony, E, Jha, P, Derop, J, Sand, O, Rabearivelo, I, Leloire, A, Pigeyre, M, Daujat-Chavanieu, M, Gerbal-Chaloin, S, Dayeh, T, Lassailly, G, Mathurin, P, Staels, B, Auwerx, J, Schurmann, A, Postic, C, Schafmayer, C, Hampe, J, Bonnefond, A, Pattou, F, Froguel, P, Metabolic functional (epi)genomics and molecular mechanisms involved in type 2 diabetes and related diseases - UMR 8199 - UMR 1283 (EGENODIA (GI3M)), 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 National de la Recherche Scientifique (CNRS), Imperial College London, Recherche translationnelle sur le diabète - U 1190 (RTD), 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), Department of Experimental Diabetology [München-Neuherberg, Germany], German Institute of Human Nutrition Potsdam-Rehbrüecke [München-Neuherberg, Germany] -Nuthetal and German Center for Diabetes Research - DZD [München-Neuherberg, Germany], German Center for Diabetes Diseases [Neuherberg, Germany] (DZD), German Institute of Human Nutrition Potsdam-Rehbrücke (DIfE), 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), Ecole Polytechnique Fédérale de Lausanne (EPFL), Cellules Souches, Plasticité Cellulaire, Médecine Régénératrice et Immunothérapies (IRMB), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM), Skane University Hospital [Malmo], Lund University [Lund], Lille Inflammation Research International Center - U 995 (LIRIC), CHU Lille, Récepteurs nucléaires, maladies cardiovasculaires et diabète - U 1011 (RNMCD), Laboratory of Integrative and Systems Physiology [Lausanne, Switzerland] (LISP), Kiel University, Technische Universität Dresden = Dresden University of Technology (TU Dresden), This study was supported by nonprofit organizations and public bodies for funding of scientific research conducted in France and within the European Union: 'Centre National de la Recherche Scientifique', 'Université de Lille 2', 'Institut Pasteur de Lille', 'Société Francophone du Diabète', 'Contrat de Plan Etat-Région', 'Agence Nationale de la Recherche', ANR-10-LABX-46, ANR EQUIPEX Ligan MP: ANR-10-EQPX-07-01, European Research Council GEPIDIAB - 294785., ANR-10-LABX-0046,EGID,EGID Diabetes Pole(2010), ANR-10-EQPX-0007,LIGAN PM,Plate forme Lilloise de séquençage du génome humain pour une médecine personnalisée(2010), European Project: 294785,EC:FP7:ERC,ERC-2011-ADG_20110310,GEPIDIAB(2012), Metabolic functional (epi)genomics and molecular mechanisms involved in type 2 diabetes and related diseases - UMR 8199 - UMR 1283 (GI3M), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre National de la Recherche Scientifique (CNRS)-Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP), Centre National de la Recherche Scientifique (CNRS)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université de Montpellier (UM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Philips, Alexandre, EGID Diabetes Pole - - EGID2010 - ANR-10-LABX-0046 - LABX - VALID, Plate forme Lilloise de séquençage du génome humain pour une médecine personnalisée - - LIGAN PM2010 - ANR-10-EQPX-0007 - EQPX - VALID, and Genetics and epigenetics of Type 2 Diabetes physiology - GEPIDIAB - - EC:FP7:ERC2012-11-01 - 2017-10-31 - 294785 - VALID

Subjects
Adult, Male, GENES, [SDV]Life Sciences [q-bio], IMATINIB MESYLATE, R.C, DISEASE, GLUCOSE, Epigenesis, Genetic, ALTERED DNA METHYLATION, ACTIVATION, PDGFA, Endocrinology & Metabolism, Non-alcoholic Fatty Liver Disease, L.Y, GLYCEMIC TRAITS, FIBROSIS, Humans, and P.F. contributed equally to the study, Genetic Predisposition to Disease, Obesity, Cells, Cultured, Platelet-Derived Growth Factor, M.C, Science & Technology, A.A, FATTY LIVER, nutritional and metabolic diseases, Type 2 diabetes, 11 Medical And Health Sciences, DNA Methylation, Middle Aged, Up-Regulation, [SDV] Life Sciences [q-bio], Diabetes Mellitus, Type 2, Liver, Case-Control Studies, Female, Epigenetics, KINASE-C-EPSILON, Insulin Resistance, Life Sciences & Biomedicine, F.P, Signal Transduction
Abstract

In type 2 diabetes (T2D), hepatic insulin resistance is strongly associated with nonalcoholic fatty liver disease (NAFLD). In this study, we hypothesized that the DNA methylome of livers from patients with T2D compared with livers of individuals with normal plasma glucose levels can unveil some mechanism of hepatic insulin resistance that could link to NAFLD. Using DNA methylome and transcriptome analyses of livers from obese individuals, we found that hypomethylation at a CpG site in PDGFA (encoding platelet-derived growth factor α) and PDGFA overexpression are both associated with increased T2D risk, hyperinsulinemia, increased insulin resistance, and increased steatohepatitis risk. Genetic risk score studies and human cell modeling pointed to a causative effect of high insulin levels on PDGFA CpG site hypomethylation, PDGFA overexpression, and increased PDGF-AA secretion from the liver. We found that PDGF-AA secretion further stimulates its own expression through protein kinase C activity and contributes to insulin resistance through decreased expression of insulin receptor substrate 1 and of insulin receptor. Importantly, hepatocyte insulin sensitivity can be restored by PDGF-AA–blocking antibodies, PDGF receptor inhibitors, and by metformin, opening therapeutic avenues. Therefore, in the liver of obese patients with T2D, the increased PDGF-AA signaling contributes to insulin resistance, opening new therapeutic avenues against T2D and possibly NAFLD.

Published
2018
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12. Prognosis of ALF of unknown cause: results of the French multicentre prospective HASIPRO study

Author

Coilly, A., primary, Dharancy, S., additional, Duvoux, C., additional, Martino, V.D., additional, Dumortier, Jérôme, additional, Radenne, S., additional, Alric, L., additional, Besch, C., additional, Francoz, C., additional, Perarnaud, J., additional, Rudler, M., additional, Carbonell, N., additional, Silvain, C., additional, Leroy, V., additional, Pichard, A.V., additional, Lassailly, G., additional, Artru, F., additional, Antonini, T., additional, Agostini, H., additional, Piedvache, C., additional, Duclos-Vallée, J.-C., additional, Ichai, P., additional, and Samuel, D., additional

Published
2018
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16. CO-16: Nouveaux marqueurs épigénétiques spécifiques du foie chez les obèses diabétiques de type 2

Author

Cauchi, S., primary, Yengo, L., additional, Canouïl, M., additional, Régent, A.S., additional, Benoit, P., additional, Lobbens, S., additional, Maillet, J., additional, Lassailly, G., additional, Caïazzo, R., additional, Raverdy, V., additional, Abderrahmani, A., additional, Ling, C., additional, Hampe, J., additional, Pattou, F., additional, and Froguel, P., additional

Published
2016
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21. Does Multiorgan Failure Impact Prognosis of Liver Transplantation in Patients with End-Stage Liver Disease? Results of a French Retrospective Multicenter Case-Control Study

Author

Artru, F., primary, Louvet, A., additional, Ruiz, I., additional, Levesque, E., additional, Labreuche, J., additional, Jaber, S., additional, Lassailly, G., additional, Dharancy, S., additional, Boleslawski, E., additional, Lebuffe, G., additional, Kipnis, E., additional, Ichai, P., additional, Coilly, A., additional, De Martin, E., additional, Vibert, E., additional, Herrerro, A., additional, Samuel, D., additional, Pageaux, G.-P., additional, Mathurin, P., additional, and Saliba, F., additional

Published
2016
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25. O139 ALCOHOLIC HEPATITIS RESISTANT TO MEDICAL THERAPY IS CHARACTERIZED BY AN ALTERED DIFFERENTIATION OF HEPATIC PROGENITORS UNDER THE INFLUENCE OF EXTRACELLULAR MATRIX

Author

Dubuquov, L., primary, Louvet, A., additional, Lassailly, G., additional, Artru, F., additional, Truant, S., additional, Maggiotto, F., additional, Gantier, E., additional, Boleslawski, E., additional, Buob, D., additional, Cannesson-Leroy, A., additional, Moreno, C., additional, Dharancy, S., additional, and Mathurin, P., additional

Published
2014
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26. FRI-449 - Does Multiorgan Failure Impact Prognosis of Liver Transplantation in Patients with End-Stage Liver Disease? Results of a French Retrospective Multicenter Case-Control Study

Author

Artru, F., Louvet, A., Ruiz, I., Levesque, E., Labreuche, J., Jaber, S., Lassailly, G., Dharancy, S., Boleslawski, E., Lebuffe, G., Kipnis, E., Ichai, P., Coilly, A., De Martin, E., Vibert, E., Herrerro, A., Samuel, D., Pageaux, G.-P., Mathurin, P., and Saliba, F.

Published
2016
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31. 100 BASELINE MODELS HELP IN IDENTIFYING RESPONDERS TO CORTICOSTEROIDS IN SEVERE ALCOHOLIC HEPATITIS: A MULTICENTER STUDY ON MORE THAN 600 PATIENTS

Author

Louvet, A., primary, Artru, F., additional, Colin, M., additional, Lassailly, G., additional, Diaz, E., additional, O'Grady, J.G., additional, Boursier, J., additional, Carithers, R.L., additional, Naveau, S., additional, Deltenre, P., additional, Canva-Delcambre, V., additional, Dharancy, S., additional, Morgan, T.R., additional, and Mathurin, P., additional

Published
2012
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32. 1301 BARIATRIC SURGERY CAN BE PROPOSED TO MORBID OBESE HIGHLY SELECTED WITH COMPENSATED CIRRHOSIS

Author

Lassailly, G., primary, Caïazzo, R., additional, Arnalsteen, L., additional, Lebuffe, G., additional, Buob, D., additional, Patrice, A., additional, Louvet, A., additional, Leteurtre, E., additional, Colin, M., additional, Dharancy, S., additional, Canva-Delcambre, V., additional, Deltenre, P., additional, Pattou, F., additional, and Mathurin, P., additional

Published
2012
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33. 6 BARIATRIC SURGERY AN EFFICIENT TREATMENT FOR PATIENT WITH STEATOHEPATITIS

Author

Lassailly, G., primary, Caïazzo, R., additional, Buob, D., additional, Arnalsteen, L., additional, Louvet, A., additional, Leteurtre, E., additional, Colin, M., additional, Dharancy, S., additional, Hollebecque, A., additional, Canva-Delcambre, V., additional, Deltenre, P., additional, Pattou, F., additional, and Mathurin, P., additional

Published
2012
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49. Intrahepatic levels of microbiome-derived hippurate associates with improved metabolic dysfunction-associated steatotic liver disease.

Author

Deslande M, Puig-Castellvi F, Castro-Dionicio I, Pacheco-Tapia R, Raverdy V, Caiazzo R, Lassailly G, Leloire A, Andrikopoulos P, Kahoul Y, Zaïbi N, Toussaint B, Oger F, Gambardella N, Lefebvre P, Derhourhi M, Amanzougarene S, Staels B, Pattou F, Froguel P, Bonnefond A, and Dumas ME

Subjects
Humans, Male, Female, Insulin Resistance, Gastrointestinal Microbiome, Middle Aged, Obesity metabolism, Obesity microbiology, Adult, Lipid Metabolism, Fatty Liver metabolism, Metabolomics methods, Metabolome, Diabetes Mellitus, Type 2 metabolism, Diabetes Mellitus, Type 2 microbiology, Liver metabolism, Hippurates metabolism
Abstract

Objective: Metabolic dysfunction-associated steatotic liver disease (MASLD) is characterised by lipid accumulation in the liver and is often associated with obesity and type 2 diabetes. The gut microbiome recently emerged as a significant player in liver metabolism and health. Hippurate, a host-microbial co-metabolite has been associated with human gut microbial gene richness and with metabolic health. However, its role on liver metabolism and homeostasis is poorly understood., Methods: We characterised liver biospies from 318 patients with obesity using RNAseq and metabolomics in liver and plasma to derive associations among hepatic hippurate, hepatic gene expression and MASLD and phenotypes. To test a potential beneficial role for hippurate in hepatic insulin resistance, we profile the metabolome of (IHH) using ultra-high-performance liquid chromatography coupled to high-resolution tandem mass spectrometry (UHPLC-MS/MS), and characterised intracellular triglyceride accumulation and glucose internalisation after a 24 h insulin exposure., Results: We first report significant associations among MASLD traits, plasma and hepatic hippurate. Further analysis of the hepatic transcriptome shows that liver and plasma hippurate are inversely associated with MASLD, implicating lipid metabolism and regulation of inflammatory responses pathways. Hippurate treatment inhibits lipid accumulation and rescues insulin resistance induced by 24-hour chronic insulin in IHH. Hippurate also improves hepatocyte metabolic profiles by increasing the abundance of metabolites involved in energy homeostasis that are depleted by chronic insulin treatment while decreasing those involved in inflammation., Conclusions: Altogether, our results further highlight hippurate as a mechanistic marker of metabolic health, by its ability to improve metabolic homeostasis as a postbiotic candidate., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2025 The Authors. Published by Elsevier GmbH.. All rights reserved.)

Published
2025
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50. Resolution of Metabolic Dysfunction-associated Steatohepatitis With No Worsening of Fibrosis After Bariatric Surgery Improves 15-year Survival: A Prospective Cohort Study.

Author

Lassailly G, Caiazzo R, Goemans A, Chetboun M, Gnemmi V, Labreuche J, Baud G, Verkindt H, Marciniak C, Oukhouya-Daoud N, Ntandja-Wandji LC, Ningarhari M, Leteurtre E, Raverdy V, Dharancy S, Louvet A, Pattou F, and Mathurin P

Abstract

Background & Aims: The aim of this study was to investigate the consequences of the histological progression of metabolic dysfunction-associated steatohepatitis (MASH) and fibrosis on long-term survival after bariatric surgery., Methods: From 1994 to 2021, 3028 patients at the University Hospital of Lille were prospectively included. Baseline liver biopsies were systematically performed with proposed follow-up biopsies 1 year after surgery, mainly in patients with MASH. We evaluated the association of the baseline and 1-year histologic progression of MASH and fibrosis status and long-term survival using Cox regression models., Results: At baseline, 2641 patients (89%) had a biopsy, including 232 with MASH (8.7%) and 266 (10.8%) with significant fibrosis (grade F2-F4). The median follow-up was 10.1 years. At 1 year, 594 patients had qualitative paired biopsies. Survival was shorter at the 15-year follow-up in patients with baseline MASH, than in those without (hazard ratio [HR], 2.21; 95% confidence interval [CI], 1.38-3.53) and in F2 to F4 than in F0 to F1 (HR, 3.38; 95% CI, 2.24-5.10). At the 1-year landmark analysis, compared with patients without baseline MASH, mortality increased in those with persistent MASH and/or if fibrosis worsened (adjusted HR, 2.54; 95% CI, 1.06-6.10), but not if MASH resolved without the worsening of fibrosis (adjusted HR, 0.73; 95% CI, 0.28-1.87). Similarly, compared with patients without significant fibrosis at baseline, patients with persistent significant fibrosis had increased mortality (adjusted HR, 4.03; 95% CI, 1.86-8.72) but not if fibrosis improved from F2 to F4 to F0 to F1 (adjusted HR; 1.49; 95% CI, 0.52-4.24)., Conclusion: Histologic remission of MASH or significant fibrosis improves survival after bariatric surgery., (Copyright © 2024 AGA Institute. Published by Elsevier Inc. All rights reserved.)

Published
2024
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