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7. The long noncoding RNA ADIPINT regulates human adipocyte metabolism via pyruvate carboxylase

Author

Kerr, A. G., Wang, Zuoneng, Wang, N., Kwok, K. H. M., Jalkanen, J., Ludzki, A., Lecoutre, S., Langin, D., Bergo, M. O., Dahlman, I., Mim, Carsten, Arner, P., Gao, H., Kerr, A. G., Wang, Zuoneng, Wang, N., Kwok, K. H. M., Jalkanen, J., Ludzki, A., Lecoutre, S., Langin, D., Bergo, M. O., Dahlman, I., Mim, Carsten, Arner, P., and Gao, H.

Abstract

The pleiotropic function of long noncoding RNAs is well recognized, but their direct role in governing metabolic homeostasis is less understood. Here, we describe a human adipocyte-specific lncRNA, ADIPINT, that regulates pyruvate carboxylase, a pivotal enzyme in energy metabolism. We developed an approach, Targeted RNA-protein identification using Orthogonal Organic Phase Separation, which identifies that ADIPINT binds to pyruvate carboxylase and validated the interaction with electron microscopy. ADIPINT knockdown alters the interactome and decreases the abundance and enzymatic activity of pyruvate carboxylase in the mitochondria. Reduced ADIPINT or pyruvate carboxylase expression lowers adipocyte lipid synthesis, breakdown, and lipid content. In human white adipose tissue, ADIPINT expression is increased in obesity and linked to fat cell size, adipose insulin resistance, and pyruvate carboxylase activity. Thus, we identify ADIPINT as a regulator of lipid metabolism in human white adipocytes, which at least in part is mediated through its interaction with pyruvate carboxylase., QC 20230227

Published
2022
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11. Coordinating Effect of VEGFC and Oleic Acid Drives Tumor Lymphangiogenesis

Author

Jérémy Nigri, Zamora A, Barbara Garmy-Susini, Anne Catherine Prats, De Toni F, Galitzky J, Jean-Emmanuel Sarry, Florent Morfoisse, Mohsen Hosseini, Bouloumié A, Richard Tomasini, Florence Tatin, Françoise Pujol, Eric Lacazette, and Langin D

Subjects
Oleic acid, chemistry.chemical_compound, chemistry, Vascular endothelial growth factor C, Cancer research, anatomy_morphology, Tumor lymphangiogenesis, Lymphangiogenesis
Abstract

In cancer, the lymphatic system is hijacked by tumor cells to escape from primary tumor and to metastasize to the sentinel lymph nodes. Tumor lymphangiogenesis is stimulated by the vascular endothelial growth factors-C (VEGFC) after binding to its receptor VEGFR-3. However, how VEGFC cooperates with other molecules to promote lymphatic neovessels growth is not fully determined. Here, we found that tumor lymphangiogenesis developed in tumoral lesions and in their surrounding adipose tissue (AT). Interestingly, lymphatic vessel density correlated with an increase of circulating free fatty acids (FFA) in the lymph from tumor-bearing mice. We found that adipocyte-released FFA are uploaded by lymphatic endothelial cells (LEC) to stimulate their sprouting. Lipidomic analysis identified the monounsaturated oleic acid (OA) as the major circulating FFA in the lymph in tumoral context. OA transporters FATP-3, -6 and CD36 were only upregulated on LEC in the presence of VEGFC showing a collaborative effect of these molecules. OA released from adipocytes is taken up by LECs to stimulate the fatty acid β-oxidation, leading to increase adipose tissue lymphangiogenesis. Our results provide new insights on the dialogue between tumors and adipocytes via the lymphatic system and identify a key role for adipocyte-derived FFA in the promotion of lymphangiogenesis, revealing novel therapeutic opportunities for inhibitors of lymphangiogenesis in cancer.

Published
2021

18. Rôle sexuellement dimorphique du récepteur aux œstrogènes ER alpha hépatocytaire dans la progression vers la stéato-hépatite métabolique

Author

Tramunt, B., Calmy, M.L., Smati, S., Alvarez-Tena, A., Polizzi, A., Al Saati, T., Bergoglio, C., Cassant-Sourdy, S., Mouisel, E., Langin, D., Haas, J., Postic, C., Guillou, H., Gourdy, P., and Montagner, A.

Abstract

Les œstrogènes, participent à la moindre susceptibilité des femmes aux hépatopathies métaboliques. Nos travaux antérieurs ont démontré que l’activité hépatocytaire du récepteur ERα, prévient le développement de la stéatose chez des souris femelles soumises à un régime hyperlipidique [1]. Néanmoins, aucune étude n’a évalué l’influence d’ERα hépatocytaire sur la progression vers la stéato-hépatite, objectif de notre étude.

Published
2024
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22. Hepatocyte-specific deletion of Pparα promotes NAFLD in the context of obesity

Author

Régnier, M., Polizzi, A., Smati, S., Lukowicz, C., Fougerat, A., Lippi, Y., Fouché, E., Lasserre, F., Naylies, C., Bétoulières, C., Barquissau, V., Mouisel, E., Bertrand-Michel, J., Batut, A., Saati, T.A., Canlet, C., Tremblay-Franco, M., Ellero-Simatos, S., Langin, D., Postic, C., Wahli, W., Loiseau, N., Guillou, H., Montagner, A., Lee Kong Chian School of Medicine (LKCMedicine), Bodescot, Myriam, Toxicité d'un contaminant alimentaire majeur, la fumonisine: rôle du métabolisme lipidique et stratégie nutritionnelle de détoxication - - Fumolip2016 - ANR-16-CE21-0003 - AAPG2016 - VALID, Impact du métabolisme des acides gras des tissus adipeux et du foie sur l'insulinorésistance - - HepAdialogue2017 - ANR-17-CE14-0015 - AAPG2017 - VALID, ToxAlim (ToxAlim), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-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-Institut National Polytechnique (Toulouse) (Toulouse INP), 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 Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Toxicologie Intégrative & Métabolisme (ToxAlim-TIM), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE)-Université Toulouse III - Paul Sabatier (UT3), 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), Transcriptomic impact of Xenobiotics (E23 TRiX), Plateforme Génome & Transcriptome (GET), Génopole Toulouse Midi-Pyrénées [Auzeville] (GENOTOUL), 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)-Génopole Toulouse Midi-Pyrénées [Auzeville] (GENOTOUL), 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)-ToxAlim (ToxAlim), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE)-Ecole d'Ingénieurs de Purpan (INPT - EI Purpan), Prévention et promotion de la cancérogénèse par les aliments (ToxAlim-PPCA), Plateforme Ezop (Ezop), 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-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)-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), Service d'Histopathologie Expérimentale [Toulouse], Metatoul AXIOM (E20 ), MetaboHUB-MetaToul, Laboratoire de Biochimie [CHU Toulouse], Institut Fédératif de Biologie (IFB), Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Pôle Biologie [CHU Toulouse], Centre Hospitalier Universitaire de Toulouse (CHU Toulouse), Institut Cochin (IC UM3 (UMR 8104 / U1016)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité), Nanyang Technological University [Singapour], Université de Lausanne = University of Lausanne (UNIL), M.R. is supported by a PhD grant from Université Paul Sabatier (Toulouse). W.W. is supported by the Lee Kong Chian School of Medicine, Nanyang Technological University Singapore start-up Grant. This work was funded by ANR 'Fumolip' and 'Hepadialogue' (to C.P,. D.L., N.L. and H.G.). S.E.-S., N.L., A.M. and H.G. are supported by the JPI HDHL - FATMAL. A.M., W.W., D.L., N.L. and H.G. were supported by Région Occitanie., ANR-16-CE21-0003,Fumolip,Toxicité d'un contaminant alimentaire majeur, la fumonisine: rôle du métabolisme lipidique et stratégie nutritionnelle de détoxication(2016), ANR-17-CE14-0015,HepAdialogue,Impact du métabolisme des acides gras des tissus adipeux et du foie sur l'insulinorésistance(2017), 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-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE)-Ecole Nationale Vétérinaire de Toulouse (ENVT), Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National des Sciences Appliquées - Toulouse (INSA Toulouse), Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Génopole Toulouse Midi-Pyrénées [Auzeville] (GENOTOUL), Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-ToxAlim (ToxAlim), MetaToul-MetaboHUB, Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-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)-Institut National de la Santé et de la Recherche Médicale (INSERM), Hôpital Purpan [Toulouse], CHU Toulouse [Toulouse]-CHU Toulouse [Toulouse], Analyse de Xénobiotiques, Identification, Métabolisme (E20 Metatoul-AXIOM), Laboratory of Clinical Biochemistry [Toulouse], CHU Toulouse [Toulouse], Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université de Paris (UP), Université de Lausanne (UNIL), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-MetaToul-MetaboHUB, and Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPC)

Subjects
Male, Systems Analysis, Metabolic disorders, lcsh:Medicine, Systems analysis, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, Diet, High-Fat, Article, Mice, Non-alcoholic Fatty Liver Disease, Animals, Humans, PPAR alpha, Medicine [Science], Obesity, lcsh:Science, [SDV.BC] Life Sciences [q-bio]/Cellular Biology, [SDV.MHEP.EM] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism, Mice, Knockout, Gene Expression Profiling, lcsh:R, nutritional and metabolic diseases, [SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism, Lipid Metabolism, Disease Models, Animal, Liver, Metabolic Disorders, Lipidomics, Hepatocytes, lcsh:Q
Abstract

Peroxisome proliferator activated receptor α (PPARα) acts as a fatty acid sensor to orchestrate the transcription of genes coding for rate-limiting enzymes required for lipid oxidation in hepatocytes. Mice only lacking Pparα in hepatocytes spontaneously develop steatosis without obesity in aging. Steatosis can develop into non alcoholic steatohepatitis (NASH), which may progress to irreversible damage, such as fibrosis and hepatocarcinoma. While NASH appears as a major public health concern worldwide, it remains an unmet medical need. In the current study, we investigated the role of hepatocyte PPARα in a preclinical model of steatosis. For this, we used High Fat Diet (HFD) feeding as a model of obesity in C57BL/6 J male Wild-Type mice (WT), in whole-body Pparα- deficient mice (Pparα-/-) and in mice lacking Pparα only in hepatocytes (Pparαhep-/-). We provide evidence that Pparα deletion in hepatocytes promotes NAFLD and liver inflammation in mice fed a HFD. This enhanced NAFLD susceptibility occurs without development of glucose intolerance. Moreover, our data reveal that non-hepatocytic PPARα activity predominantly contributes to the metabolic response to HFD. Taken together, our data support hepatocyte PPARα as being essential to the prevention of NAFLD and that extra-hepatocyte PPARα activity contributes to whole-body lipid homeostasis. Nanyang Technological University Published version We thank all members of the EZOP staff for their careful help from the early start of this project. We thank Léa Morra-Charrot and Laurent Monbrun from Anexplo for their excellent work on plasma biochemistry. We thank the staff from the Genotoul: Anexplo, GeT-TRiX and Metatoul-Lipidomic facilities. The authors wish to thank Pr Daniel Metzger, Pr Pierre Chambon (IGBMC, Illkirch, France) and the staff of the Mouse Clinical Institute (Illkirch, France) for their critical support in this project. We thank Pr Didier Trono (EPFL, Lausanne, Switzerland) for providing the Albumin-Cre mice. We thank Dr Joel Haas, Pr Bart Staels and Dr Thierry Pineau for constructive discussions. We thank Dr Thierry Pineau for providing us with Pparα-null mice. M.R. is supported by a PhD grant from Université Paul Sabatier (Toulouse). W.W. is supported by the Lee Kong Chian School of Medicine, Nanyang Technological University Singapore start-up Grant. This work was funded by ANR “Fumolip” and “Hepadialogue” (to C.P,. D.L., N.L. and H.G.). S.E.-S., N.L., A.M. and H.G. are supported by the JPI HDHL - FATMAL. A.M., W.W., D.L., N.L. and H.G. were supported by Région Occitanie.

Published
2020

25. The atrial natriuretic peptide- and catecholamine-induced lipolysis and expression of related genes in adipose tissue in hypothyroid and hyperthyroid patients

Author

Polak, J., Moro, C., Klimcakova, E., Kovacikova, M., Bajzova, M., Vitkova, M., Kovacova, Z., Sotornik, R., Berlan, M., Viguerie, N., Langin, D., and Stich, V.

Subjects
Thyroid diseases -- Research, Metabolic diseases -- Research, Lipolysis -- Research, Adipose tissues -- Research, Biological sciences
Abstract

Thyroid dysfunction is associated with several abnormalities in intermediary metabolism, including impairment of lipolytic response to catecholamines in subcutaneous abdominal adipose tissue (SCAAT). Atrial natriuretic peptide (ANP) is a powerful lipolytic peptide; however, the role of ANP-mediated lipolysis in thyroid disease has not been elucidated. The aim of this study was to investigate the role of thyroid hormones in the regulation of ANP-induced lipolysis as well as in the gene expression of hormone-sensitive lipase, phosphodiesterase 3B (PDE3B), uncoupling protein-2 (UCP2), natriuretic peptide receptor type A, and [[beta].sub.2]-adrenergic receptor in SCAAT of hyperthyroid and hypothyroid patients. Gene expression in SCAAT was studied in 13 hypothyroid and 11 hyperthyroid age-matched women before and 2-4 mo after the normalization of their thyroid status. A microdialysis study was performed on a subset of nine hyperthyroid and 10 hypothyroid subjects. ANP- and isoprenaline-induced lipolyses were higher in hyperthyroid subjects, with no differences between the groups following treatment. Hormone-sensitive lipase gene expression was higher in hyperthyroid compared with hypothyroid subjects before treatment, whereas no difference was observed following treatment. No differences in gene expression of other genes were observed between the two groups. Following treatment, the gene expression of UCP2 decreased in hyperthyroid, whereas the expression of PDE3B decreased in hypothyroid subjects. We conclude that thyroid hormones regulate ANP- and isoprenaline-mediated lipolysis in human SCAAT in vivo. Increased lipolytic subcutaneous adipose tissue response in hyperthyroid patients may involve postreceptor signaling mechanisms. adrenergic lipolysis; thyroid disease; gene expression doi:10.1152/ajpendo.00688.2007

Published
2007

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