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1. Multi-Omics Data Integration Reveals Sex-Dependent Hippocampal Programming by Maternal High-Fat Diet during Lactation in Adult Mouse Offspring

Author

Gauvrit, Thibaut, primary, Benderradji, Hamza, additional, Pelletier, Alexandre, additional, Aboulouard, Soulaimane, additional, Faivre, Emilie, additional, Carvalho, Kévin, additional, Deleau, Aude, additional, Vallez, Emmanuelle, additional, Launay, Agathe, additional, Bogdanova, Anna, additional, Besegher, Mélanie, additional, Le Gras, Stéphanie, additional, Tailleux, Anne, additional, Salzet, Michel, additional, Buée, Luc, additional, Delahaye, Fabien, additional, Blum, David, additional, and Vieau, Didier, additional

Published
2023
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2. Tau, Diabetes and Insulin

Author

Gratuze, Maud, Joly-Amado, Aurélie, Buee, Luc, Vieau, Didier, Blum, David, Crusio, Wim E., Series Editor, Lambris, John D., Series Editor, Radeke, Heinfried H., Series Editor, Rezaei, Nima, Series Editor, Takashima, Akihiko, editor, Wolozin, Benjamin, editor, and Buee, Luc, editor

Published
2019
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3. Caffeine intake exerts dual genome-wide effects on hippocampal metabolism and learning-dependent transcription

Author

Paiva, Isabel, Cellai, Lucrezia, Meriaux, Celine, Poncelet, Lauranne, Nebie, Ouada, Saliou, Jean-Michel, Lacoste, Anne-Sophie, Papegaey, Anthony, Drobecq, Herve, Gras, Stephanie Le, Schneider, Marion, Malik, Enas M., Muller, Christa E., Faivre, Emilie, Carvalho, Kevin, Gomez-Murcia, Victoria, Vieau, Didier, Thiroux, Bryan, Eddarkaoui, Sabiha, Lebouvier, Thibaud, Schueller, Estelle, Tzeplaeff, Laura, Grgurina, Iris, Seguin, Jonathan, Stauber, Jonathan, Lopes, Luisa V., Buee, Luc, Buee-Scherrer, Valerie, Cunha, Rodrigo A., Ait-Belkacem, Rima, Sergean, Nicolas, Annicotte, Jean-Sebastien, Boutillier, Anne-Laurence, and Blum, David

Subjects
Hippocampus (Brain) -- Physiological aspects -- Health aspects -- Genetic aspects, Metabolism -- Genetic aspects -- Health aspects, Neural transmission -- Health aspects -- Genetic aspects, Caffeine -- Health aspects -- Physiological aspects -- Genetic aspects, Health care industry
Abstract

Caffeine is the most widely consumed psychoactive substance in the world. Strikingly, the molecular pathways engaged by its regular consumption remain unclear. We herein addressed the mechanisms associated with habitual (chronic) caffeine consumption in the mouse hippocampus using untargeted orthogonal omics techniques. Our results revealed that chronic caffeine exerts concerted pleiotropic effects in the hippocampus at the epigenomic, proteomic, and metabolomic levels. Caffeine lowered metabolism-related processes (e.g., at the level of metabolomics and gene expression) in bulk tissue, while it induced neuron-specific epigenetic changes at synaptic transmission/plasticity-related genes and increased experience-driven transcriptional activity. Altogether, these findings suggest that regular caffeine intake improves the signal-to-noise ratio during information encoding, in part through fine-tuning of metabolic genes, while boosting the salience of information processing during learning in neuronal circuits., Introduction Caffeine is the most widely consumed psychoactive substance in the world (by about 80% of the population) via dietary intake from coffee, tea, and soda beverages. Its popularity derives [...]

Published
2022
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11. Impaired Glucose Homeostasis in a Tau Knock-In Mouse Model

Author

Benderradji, Hamza, primary, Kraiem, Sarra, additional, Courty, Emilie, additional, Eddarkaoui, Sabiha, additional, Bourouh, Cyril, additional, Faivre, Emilie, additional, Rolland, Laure, additional, Caron, Emilie, additional, Besegher, Mélanie, additional, Oger, Frederik, additional, Boschetti, Theo, additional, Carvalho, Kévin, additional, Thiroux, Bryan, additional, Gauvrit, Thibaut, additional, Nicolas, Emilie, additional, Gomez-Murcia, Victoria, additional, Bogdanova, Anna, additional, Bongiovanni, Antonino, additional, Muhr-Tailleux, Anne, additional, Lancel, Steve, additional, Bantubungi, Kadiombo, additional, Sergeant, Nicolas, additional, Annicotte, Jean-Sebastien, additional, Buée, Luc, additional, Vieau, Didier, additional, Blum, David, additional, and Buée-Scherrer, Valérie, additional

Published
2022
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13. P2X7-deficiency improves plasticity and cognitive abilities in a mouse model of Tauopathy

Author

Carvalho, Kevin, primary, Martin, Elodie, additional, Ces, Aurélia, additional, Sarrazin, Nadège, additional, Lagouge-Roussey, Pauline, additional, Nous, Caroline, additional, Boucherit, Leyna, additional, Youssef, Ihsen, additional, Prigent, Annick, additional, Faivre, Emilie, additional, Eddarkaoui, Sabiha, additional, Gauvrit, Thibaut, additional, Vieau, Didier, additional, Boluda, Susana, additional, Huin, Vincent, additional, Fontaine, Bertrand, additional, Buée, Luc, additional, Delatour, Benoît, additional, Dutar, Patrick, additional, Sennlaub, Florian, additional, Guillonneau, Xavier, additional, Blum, David, additional, and Delarasse, Cécile, additional

Published
2021
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15. Maternal perinatal undernutrition programs a 'brown-like' phenotype of gonadal white fat in male rat at weaning

Author

Delahaye, Fabien, Lukaszewski, Marie-Amelie, Wattez, Jean-Sebastien, Cisse, Ouma, Dutriez-Casteloot, Isabelle, Fajardy, Isabelle, Montel, Valerie, Diekes-Coopman, Anne, Laborie, Christine, Lesage, Jean, Breton, Christophe, and Vieau, Didier

Subjects
Gene expression -- Physiological aspects, Neuropeptide Y -- Properties, Phenotype -- Identification and classification, Adipose tissues -- Genetic aspects, Biological sciences
Abstract

Several studies indicate that maternal undernutrition sensitizes the offspring to the development of metabolic disorders, such as obesity. Using a model of perinatal maternal 50% food-restricted diet (FR50), we recently reported that rat neonates from undernourished mothers exhibit decreased leptin plasma levels associated with alterations of hypothalamic proopiomelanocortin system. The present study aimed at examining the consequences of FR50 on the brain-adipose axis in male rat neonates. Using quantitative RT-PCR array containing 84 obesity-related genes, we demonstrated that most of the genes involved in energy metabolism regulation are expressed in rat gonadal white adipose tissue (WAT) and are sensitive to maternal perinatal undernutrition (MPU). In contrast, hypothalamic gene expression was not substantially affected by MPU. Gene expression of uncoupling protein 1 (UCP1), a marker of brown adipocytes, showed an almost 400-fold stimulation in postnatal day 21 (PND21) FR50 animals, suggesting that their gonadal WAT possesses a brown-like phenotype. This was confirmed by histological and immunoshistochemical procedures, which demonstrated that PND21 FR50 gonadal adipocytes are multilocular, resembling those present in interscapular brown adipose tissue, and exhibit an overexpression of UCP1 and neuropeptide Y (NPY) at the protein level. Control animals contained almost exclusively 'classical' unilocular white adipocytes that did not show high UCP1 and NPY labeling. After weaning, FR50 animals exhibited a transient hyperphagia that was associated with the disappearance of brown-like fat pads in PND30 WAT. Our results demonstrate that MPU delays the maturation of gonadal WAT during critical developmental time windows, suggesting that it could have long-term consequences on body weight regulation in the offspring. maternal undernutrition; neuropeptide Y; uncoupling protein 1; peroxisome proliferator-activated receptor-[gamma] coactivator-1[alpha]; adipose tissue programming doi: 10.1152/ajpregu.00604.2009.

Published
2010

16. Maternal prenatal undernutrition alters the response of POMC neurons to energy status variation in adult male rat offspring

Author

Breton, Christophe, Lukaszewski, Marie-Amelie, Risold, Pierre-Yves, Enache, Mihaela, Guillemot, Johann, Riviere, Guillaume, Delahaye, Fabien, Lesage, Jean, Dutriez-Casteloot, Isabelle, Laborie, Christine, and Vieau, Didier

Subjects
Fetal malnutrition -- Complications and side effects, Appetite -- Management, Hypothalamus -- Properties, Neurons -- Properties, Company business management, Biological sciences
Abstract

Epidemiological studies suggest that maternal undernutrition predisposes the offspring to development of energy balance metabolic pathologies in adulthood. Using a model of a prenatal maternal 70% food-restricted diet (FR30) in rats, we evaluated peripheral parameters involved in nutritional regulation, as well as the hypothalamic appetite-regulatory system, in nonfasted and 48-h-fasted adult offspring. Despite comparable glycemia in both groups, mild glucose intolerance, with a defect in glucose-induced insulin secretion, was observed in FR30 animals. They also exhibited hyperleptinemia, despite similar visible fat deposits. Using semiquantitative RT-PCR, we observed no basal difference of hypothalamic proopiomelanocortin (POMC) and neuropeptide Y (NPY) gene expression, but a decrease of the OB-Rb and an increase of insulin receptor mRNA levels, in FR30 animals. These animals also exhibited basal hypercorticosteronemia and a blunted increase of corticosterone in fasted compared with control animals. After fasting, FR30 animals showed no marked reduction of POMC mRNA levels or intensity of [beta]-endorphin-immunoreactive fiber projections. By contrast, NPY gene expression and immunoreactive fiber intensity increased. FR30 rats also displayed subtle alterations of food intake: body weight-related food intake was higher and light-dark phase rhythm and refeeding time course were modified after fasting. At rest, in the morning, hyperinsulinemia and a striking increase in the number of c-Fos-containing cells in the arcuate nucleus were observed. About 30% of the c-Fos-expressing cells were POMC neurons. Our data suggest that maternal undernutrition differently programs the long-term appetite-regulatory system of offspring, especially the response of POMC neurons to energy status and food intake rhythm. maternal undernutrition; appetite programming; hypothalamus; arcuate nucleus; feeding rhythm

Published
2009

18. Maternal stress alters endocrine function of the feto-placental unit in rats

Author

Mairesse, Jerome, Lesage, Jean, Breton, Christophe, Breant, Bernadette, Hahn, Tom, Darnaudery, Muriel, Dickson, Suzanne L., Seckl, Jonathan, Biondeau, Bertrand, Vieau, Didier, Maccari, Stefania, and Viltart, Odile

Subjects
ACTH -- Research, Placenta -- Research, Prenatal influences -- Research, Somatotropin -- Research, Biological sciences
Abstract

Prenatal stress (PS) can cause early and long-term developmental effects resulting in part from altered maternal and/or fetal glucocorticoid exposure. The aim of the present study was to assess the impact of chronic restraint stress during late gestation on feto-placental unit physiology and function in embryonic (E) day 21 male rat fetuses. Chronic stress decreased body weight gain and food intake of the dams and increased their adrenal weight. In the placenta of PS rats, the expression of glucose transporter type 1 (GLUT1) was decreased, whereas GLUT3 and GLUT4 were slightly increased. Moreover, placental expression and activity of the glucocorticoid 'barrier' enzyme 11[beta]-hydroxysteroid dehydrogenase type 2 was strongly reduced. At E21, PS fetuses exhibited decreased body, adrenal pancreas, and testis weights. These alterations were associated with reduced pancreatic [beta]-cell mass, plasma levels of glucose, growth hormone, and ACTH, whereas corticosterone, insulin, IGF-1, and CBG levels were unaffected. These data emphasize the impact of PS on both fetal growth and endocrine function as well as on placental physiology, suggesting that PS could program processes implied in adult biology and pathophysiology. prenatal stress; placenta; adrenal; testis; pancreas; glucose; growth hormone; adrenocorticotropic hormone doi:10.1152/ajpendo.00574.2006

Published
2007

20. Maternal obesity programs increased leptin gene expression in rat male offspring via epigenetic modifications in a depot-specific manner

Author

Lecoutre, Simon, Oger, Frederik, Pourpe, Charlène, Butruille, Laura, Marousez, Lucie, Dickes-Coopman, Anne, Laborie, Christine, Guinez, Céline, Lesage, Jean, Vieau, Didier, Junien, Claudine, Eberlé, Delphine, Gabory, Anne, Eeckhoute, Jérôme, Breton, Christophe, Environnement périnatal et croissance, Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Biologie du développement et reproduction (BDR), École nationale vétérinaire d'Alfort (ENVA)-Institut National de la Recherche Agronomique (INRA)-Centre National de la Recherche Scientifique (CNRS), Université Paris-Saclay, Université de Versailles Saint-Quentin-en-Yvelines (UVSQ), Récepteurs nucléaires, maladies cardiovasculaires et diabète (EGID), Université de Lille, Droit et Santé-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Université de Lille, Centre Hospitalier Universitaire de Lille (CHU de Lille), French 'Heart and Arteries' Foundation (FCA13T1), Fondation pour la Recherche Médicale (DEQ20150331724), European Genomic Institute for Diabetes (E.G.I.D, ANR-10-LABX-46), Environnement périnatal et croissance - EA 4489 (EPS), Biologie du Développement et Reproduction (BDR), École nationale vétérinaire - Alfort (ENVA)-Institut National de la Recherche Agronomique (INRA), 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), École nationale vétérinaire d'Alfort (ENVA)-Institut National de la Recherche Agronomique (INRA), and 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)

Subjects
Leptin, Male, obesity, lcsh:Internal medicine, expression génique, Epigenetic mechanisms, Adipose Tissue, White, tissu adipeux, Adipose tissue, Brief Communication, Epigenesis, Genetic, épigénétique, Pregnancy, Animals, Developmental origin of health and disease, Fat expansion, Gene expression, Perinatal programming, Rats, Wistar, lcsh:RC31-1245, [SDV.BDD]Life Sciences [q-bio]/Development Biology, Biologie du développement, DNA Methylation, immunoprecipitation reaction, Development Biology, Rats, Up-Regulation, Histone Code, Pregnancy Complications, obésité, modification épigénique, leptine, chromatin, Female, chromatine, immunoprécipitation
Abstract

Objective According to the Developmental Origin of Health and Disease (DOHaD) concept, maternal obesity and accelerated growth in neonates predispose offspring to white adipose tissue (WAT) accumulation. In rodents, adipogenesis mainly develops during lactation. The mechanisms underlying the phenomenon known as developmental programming remain elusive. We previously reported that adult rat offspring from high-fat diet-fed dams (called HF) exhibited hypertrophic adipocyte, hyperleptinemia and increased leptin mRNA levels in a depot-specific manner. We hypothesized that leptin upregulation occurs via epigenetic malprogramming, which takes place early during development of WAT. Methods As a first step, we identified in silico two potential enhancers located upstream and downstream of the leptin transcription start site that exhibit strong dynamic epigenomic remodeling during adipocyte differentiation. We then focused on epigenetic modifications (methylation, hydroxymethylation, and histone modifications) of the promoter and the two potential enhancers regulating leptin gene expression in perirenal (pWAT) and inguinal (iWAT) fat pads of HF offspring during lactation (postnatal days 12 (PND12) and 21 (PND21)) and in adulthood. Results PND12 is an active period for epigenomic remodeling in both deposits especially in the upstream enhancer, consistent with leptin gene induction during adipogenesis. Unlike iWAT, some of these epigenetic marks were still observable in pWAT of weaned HF offspring. Retained marks were only visible in pWAT of 9-month-old HF rats that showed a persistent “expandable” phenotype. Conclusions Consistent with the DOHaD hypothesis, persistent epigenetic remodeling occurs at regulatory regions especially within intergenic sequences, linked to higher leptin gene expression in adult HF offspring in a depot-specific manner., Highlights • The white adipose tissue is an important target of developmental programming. • Higher leptin gene expression occurs in offspring from obese dams in a depot-specific manner. • Leptin upregulation occurs via epigenetic malprogramming during development of adipose tissue. • Persistent genomic epigenetic remodeling occurs in adipose tissue of offspring from obese dams. • Intergenic regions were more affected than the leptin promoter region in offspring of obese dams.

Published
2017

29. Transcription profiling in the liver of undernourished male rat offspring reveals altered lipid metabolism pathways and predisposition to hepatic steatosis

Author

Lecoutre, Simon, primary, Montel, Valérie, additional, Vallez, Emmanuelle, additional, Pourpe, Charlène, additional, Delmont, Anne, additional, Eury, Elodie, additional, Verbanck, Marie, additional, Dickes-Coopman, Anne, additional, Daubersies, Pierre, additional, Lesage, Jean, additional, Laborie, Christine, additional, Tailleux, Anne, additional, Staels, Bart, additional, Froguel, Philippe, additional, Breton, Christophe, additional, and Vieau, Didier, additional

Published
2019
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31. [Brain insulin signaling and Tau: impact for Alzheimer's disease and Tauopathies]

Author

Joly-Amado, Aurélie, Gratuze, Maud, Benderradji, Hamza, Vieau, Didier, Buee, Luc, Blum, David, Department of Molecular Pharmacology and Physiology [Tampa, FL, USA] (Byrd Alzheimer’s Institute ), University of South Florida [Tampa] (USF), Axe Neurosciences [CHU Québec], Centre Hospitalier Université Laval [Quebec] (CHUL), CHU de Québec–Université Laval, Université Laval [Québec] (ULaval)-Université Laval [Québec] (ULaval)-CHU de Québec–Université Laval, Université Laval [Québec] (ULaval)-Université Laval [Québec] (ULaval)-Centre de recherche du CHU de Québec-Université Laval (CRCHUQ), Université Laval [Québec] (ULaval)-Université Laval [Québec] (ULaval), Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer - U1172 Inserm - U837 (JPArc), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Lille Nord de France (COMUE)-Université de Lille, and Excellence Laboratory LabEx DISTALZ

Subjects
Tauopathies, Alzheimer Disease, Animals, Brain, Humans, Insulin, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], tau Proteins, Insulin Resistance, Cognition Disorders, Signal Transduction
Abstract

International audience; Alzheimer's disease (AD) is a neurodegenerative disease primarily characterized by cognitive deficits and neuropathological lesions such as Tau aggregates and amyloid plaques, but also associated with metabolic and neuroendocrine abnormalities, such as impairment of cerebral insulin. However, the origin of these symptoms and their relationship to pathology and cognitive disorders remain poorly understood. Insulin is a hormone involved in the control of peripheral and central energy homeostasis, and insulin-resistant state has been linked to increased risk of dementia. It is now well established that brain insulin resistance can exacerbate Tau lesions. Conversely, recent data indicate that Tau protein can modulate insulin signalling in the brain, creating a vicious circle precipitating the pathological AD. This review aims to highlight our current understanding of the role of insulin in the brain and its relationship with Tau protein in the context of AD and Tauopathies.; La maladie d’Alzheimer (MA) est une maladie neurodégénérative caractérisée par des déficits cognitifs et des lésions (agrégats de Tau et plaques amyloïdes), mais également par des troubles métaboliques et neuroendocriniens. Les mécanismes à l’origine de ces processus physiopathologiques demeurent mal compris mais pourraient provenir du développement d’une insulino-résistance centrale. L’altération de l’action de l’insuline dans le cerveau des patients atteints de MA a été décrite comme facteur aggravant les lésions Tau et amyloïdes ainsi que les troubles cognitifs. L’origine de cette résistance centrale est bien moins comprise mais ferait intervenir la protéine Tau, suggérant l’existence d’un cercle vicieux contribuant à l’apparition et à la progression des signes cliniques. La présente revue vise à faire le point sur notre compréhension actuelle du rôle de l’insuline dans le cerveau et de sa relation avec la protéine Tau dans la MA et les Tauopathies.

Published
2018

37. L’interdisciplinarité au service de l’environnement (Journée d’études, université d’Artois, Arras, 3 février 2017)

Author

Petit, Olivier, Coget, Jacques, Hinnewinkel, Christelle, Moulin, David, Vergne, Virginie, Vieau, Didier, Centre Lillois d’Études et de Recherches Sociologiques et Économiques - UMR 8019 (CLERSÉ), Centre National de la Recherche Scientifique (CNRS)-Université de Lille, Territoires, Villes, Environnement & Société - ULR 4477 (TVES), Université du Littoral Côte d'Opale (ULCO)-Université de Lille, Histoire Archéologie Littérature des Mondes Anciens - UMR 8164 (HALMA), Université de Lille-Centre National de la Recherche Scientifique (CNRS)-Ministère de la Culture (MC), Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer - U1172 Inserm - U837 (JPArc), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Lille Nord de France (COMUE)-Université de Lille, Université de Lille, CNRS, Univ. Littoral Côte d’Opale, Territoires, Villes, Environnement & Société (TVES) - ULR 4477, Centre Lillois d’Études et de Recherches Sociologiques et Économiques - UMR 8019 [CLERSÉ], Territoires, Villes, Environnement & Société - ULR 4477 [TVES], Histoire Archéologie Littératures des Mondes Anciens (HALMA) - UMR 8164, Environnement Périnatal et Santé - EA 4489, Histoire, Archéologie et Littérature des Mondes Anciens - UMR 8164 [HALMA], Université de Lille-Centre National de la Recherche Scientifique (CNRS), Histoire, Archéologie et Littérature des Mondes Anciens - UMR 8164 (HALMA), Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer - U837 (JPArc), and Université Lille Nord de France (COMUE)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille

Subjects
[SHS.ENVIR]Humanities and Social Sciences/Environmental studies, ComputingMilieux_MISCELLANEOUS
Abstract

International audience

Published
2018

38. L’interdisciplinarité au service de l’environnement . Compte rendu de journée d’études, université d’Artois, Arras, 3 février 2017

Author

Petit, Olivier, Coget, Jacques, Hinnewinkel, Christelle, Moulin, David, Vergne, Virginie, Vieau, Didier, Centre Lillois d’Études et de Recherches Sociologiques et Économiques - UMR 8019 (CLERSE), Université de Lille-Centre National de la Recherche Scientifique (CNRS), Conseil Scientifique de l'Environnement Nord - Pas-de-Calais [Lille] (CSENPC), Territoires, Villes, Environnement & Société - ULR 4477 (TVES), Université du Littoral Côte d'Opale (ULCO)-Université de Lille, Espaces naturels régionaux [Lille] (ENRx), Histoire Archéologie Littérature des Mondes Anciens - UMR 8164 (HALMA), Ministère de la Culture (MC)-Université de Lille-Centre National de la Recherche Scientifique (CNRS), Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer - U1172 Inserm - U837 (JPArc), Centre National de la Recherche Scientifique (CNRS)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Université Lille Nord de France (COMUE)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université de Lille-Université du Littoral Côte d'Opale (ULCO), Université de Lille-Centre National de la Recherche Scientifique (CNRS)-Ministère de la Culture (MC), and Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Lille Nord de France (COMUE)-Université de Lille

Subjects
[SHS.ENVIR]Humanities and Social Sciences/Environmental studies
Published
2018

39. A 2A R‐induced transcriptional deregulation in astrocytes: An in vitro study

Author

Paiva, Isabel, primary, Carvalho, Kévin, additional, Santos, Patrícia, additional, Cellai, Lucrezia, additional, Pavlou, Maria Angeliki S., additional, Jain, Gaurav, additional, Gnad, Thorsten, additional, Pfeifer, Alexander, additional, Vieau, Didier, additional, Fischer, André, additional, Buée, Luc, additional, Outeiro, Tiago F., additional, and Blum, David, additional

Published
2019
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40. Brain insulin response and peripheral metabolic changes in a Tau transgenic mouse model

Author

Leboucher, Antoine, primary, Ahmed, Tariq, additional, Caron, Emilie, additional, Tailleux, Anne, additional, Raison, Sylvie, additional, Joly-Amado, Aurélie, additional, Marciniak, Elodie, additional, Carvalho, Kevin, additional, Hamdane, Malika, additional, Bantubungi, Kadiombo, additional, Lancel, Steve, additional, Eddarkaoui, Sabiha, additional, Caillierez, Raphaelle, additional, Vallez, Emmanuelle, additional, Staels, Bart, additional, Vieau, Didier, additional, Balschun, Detlef, additional, Buee, Luc, additional, and Blum, David, additional

Published
2019
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41. Tau deletion promotes brain insulin resistance

Author

Marciniak, Elodie, Leboucher, Antoine, Caron, Emilie, Ahmed, Tariq, Tailleux, Anne, Dumont, Julie, Issad, Tarik, Gerhardt, Ellen, Pagesy, Patrick, Vileno, Margaux, Bournonville, Clément, Hamdane, Malika, Bantubungi, Kadiombo, Lancel, Steve, Demeyer, Dominique, Eddarkaoui, Sabiha, Vallez, Emmanuelle, Vieau, Didier, Humez, Sandrine, Faivre, Emilie, Grenier-Boley, Benjamin, Outeiro, Tiago F., Staels, Bart, Amouyel, Philippe, Balschun, Detlef, Buee, Luc, Blum, David, Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer - U1172 Inserm - U837 (JPArc), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Lille Nord de France (COMUE)-Université de Lille, Laboratory of Biological Psychology, Catholic University of Leuven - Katholieke Universiteit Leuven (KU Leuven), 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)-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)), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Neuroendocrinologie et physiopathologie neuronale, Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille, Droit et Santé, Impact de l'environnement chimique sur la santé humaine - ULR 4483 (IMPECS), Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Unité Neurosciences et Physiologie Adaptative, Université de Lille, Sciences et Technologies, STMicroelectronics [Rousset] (ST-ROUSSET), Epidémiologie des maladies chroniques : impact des interactions gène environnement sur la santé des populations, 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, Droit et Santé, Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer - U837 (JPArc), Université Lille Nord de France (COMUE)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université 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), and Blum, David

Subjects
[SDV.MHEP.EM] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism, Male, Mice, Knockout, Brief Definitive Report, Brain, tau Proteins, [SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism, Hippocampus, Mice, Inbred C57BL, Mice, Haplotypes, mental disorders, Animals, Humans, Insulin, Cognitive Dysfunction, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], [SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], Insulin Resistance, Research Articles, ComputingMilieux_MISCELLANEOUS
Abstract

Physiological functions of tau remain ill defined. In the present study, Marciniak et al. uncover a novel function of tau in its ability to regulate brain insulin signaling and discuss the pathophysiological implications of these findings for Alzheimer’s disease and tauopathies., The molecular pathways underlying tau pathology–induced synaptic/cognitive deficits and neurodegeneration are poorly understood. One prevalent hypothesis is that hyperphosphorylation, misfolding, and fibrillization of tau impair synaptic plasticity and cause degeneration. However, tau pathology may also result in the loss of specific physiological tau functions, which are largely unknown but could contribute to neuronal dysfunction. In the present study, we uncovered a novel function of tau in its ability to regulate brain insulin signaling. We found that tau deletion leads to an impaired hippocampal response to insulin, caused by altered IRS-1 and PTEN (phosphatase and tensin homologue on chromosome 10) activities. Our data also demonstrate that tau knockout mice exhibit an impaired hypothalamic anorexigenic effect of insulin that is associated with energy metabolism alterations. Consistently, we found that tau haplotypes are associated with glycemic traits in humans. The present data have far-reaching clinical implications and raise the hypothesis that pathophysiological tau loss-of-function favors brain insulin resistance, which is instrumental for cognitive and metabolic impairments in Alzheimer’s disease patients.

Published
2017

48. Reduced PPARγ2 expression in adipose tissue of male rat offspring from obese dams is associated with epigenetic modifications

Author

Lecoutre, Simon, primary, Pourpe, Charlène, additional, Butruille, Laura, additional, Marousez, Lucie, additional, Laborie, Christine, additional, Guinez, Ce´line, additional, Lesage, Jean, additional, Vieau, Didier, additional, Eeckhoute, Je´rome, additional, Gabory, Anne, additional, Oger, Fre´de´rik, additional, Eberle´, Delphine, additional, and Breton, Christophe, additional

Published
2018
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