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1. Microbial-Host Co-metabolites Are Prodromal Markers Predicting Phenotypic Heterogeneity in Behavior, Obesity, and Impaired Glucose Tolerance

Author

Dumas, Marc-Emmanuel, Rothwell, Alice R., Hoyles, Lesley, Aranias, Thomas, Chilloux, Julien, Calderari, Sophie, Noll, Elisa M., Péan, Noémie, Boulangé, Claire L., Blancher, Christine, Barton, Richard H., Gu, Quan, Fearnside, Jane F., Deshayes, Chloé, Hue, Christophe, Scott, James, Nicholson, Jeremy K., and Gauguier, Dominique

Published
2017
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2. Intestinal invalidation of the glucose transporter GLUT2 delays tissue distribution of glucose and reveals an unexpected role in gut homeostasis

Author

Schmitt, Charlotte C., Aranias, Thomas, Viel, Thomas, Chateau, Danielle, Le Gall, Maude, Waligora-Dupriet, Anne-Judith, Melchior, Chloé, Rouxel, Ophélie, Kapel, Nathalie, Gourcerol, Guillaume, Tavitian, Bertrand, Lehuen, Agnès, Brot-Laroche, Edith, Leturque, Armelle, Serradas, Patricia, and Grosfeld, Alexandra

Published
2017
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4. Additional file 1: of Metabolic retroconversion of trimethylamine N-oxide and the gut microbiota

Author

Hoyles, Lesley, Jiménez-Pranteda, Maria, Chilloux, Julien, Francois Brial, Myridakis, Antonis, Aranias, Thomas, Magnan, Christophe, Gibson, Glenn, Sanderson, Jeremy, Nicholson, Jeremy, Gauguier, Dominique, McCartney, Anne, and Marc-Emmanuel Dumas

Abstract

Figure S1. Effect of TMAO on mixed faecal microbial population in vitro. Enumeration of bacteria in fermentation vessels by FISH analysis. Red lines, TMAO-containing systems; blue lines, negative controls. Data are shown as mean + SD (n = 3). Eub338, total bacteria; Bac303, Bacteroidales; Ato291, “Atopobium cluster”; Bif164, Bifidobacterium spp.; Ent, Enterobacteriaceae; Bet42a, Betaproteobacteria; Prop853, Veillonellaceae; Lab158, lactic acid bacteria (Lactobacillales); Fpra655, Faecalibacterium prausnitzii and Subdoligranulum spp.; Erec482, Lachnospiraceae; Clit135, Clostridium cluster XI; Rbro730/Rfla729, Ruminococcaceae; Chis150, Clostridium clusters I and II. Detection limit of the method was 4.95 log10 (number of bacteria/mL sample). *Statistically significantly different (adjusted P

Published
2018
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5. Microbial-host co-metabolites are prodromal markers predicting phenotypic heterogeneity in behavior, obesity, and impaired glucose tolerance

Author

Hoyles, Lesley, Aranias, Thomas, Chilloux, Julien, Calderari, Sophie, Noll, Elisa M., Péan, Noémie, Boulangé, Claire L., Blancher, Christine, Barton, Richard H., Gu, Quan, Fearnside, Jane F., Deshayes, Chloé, Hue, Christophe, Scott, James, Nicholson, Jeremy K, Gauguier, Dominique, Dumas, Marc-Emmanuel, and Rothwell, Alice R.

Subjects
anxiete, obésité, sécrétion d'insuline, TMAO, anxiety, endoplasmic reticulum stress, impaired glucose tolerance, insulin secretion, metabolome, microbiome, natural phenotypic variation, obesity, transcriptome, trimethylamine-N-oxide, Biologie du développement, Development Biology
Abstract

The influence of the gut microbiome on metabolic and behavioral traits is widely accepted, though the microbiome-derived metabolites involved remain unclear. We carried out untargeted urine (1)H-NMR spectroscopy-based metabolic phenotyping in an isogenic C57BL/6J mouse population (n = 50) and show that microbial-host co-metabolites are prodromal (i.e., early) markers predicting future divergence in metabolic (obesity and glucose homeostasis) and behavioral (anxiety and activity) outcomes with 94%-100% accuracy. Some of these metabolites also modulate disease phenotypes, best illustrated by trimethylamine-N-oxide (TMAO), a product of microbial-host co-metabolism predicting future obesity, impaired glucose tolerance (IGT), and behavior while reducing endoplasmic reticulum stress and lipogenesis in 3T3-L1 adipocytes. Chronic in vivo TMAO treatment limits IGT in HFD-fed mice and isolated pancreatic islets by increasing insulin secretion. We highlight the prodromal potential of microbial metabolites to predict disease outcomes and their potential in shaping mammalian phenotypic heterogeneity.

Published
2017

6. Metabolic retroconversion of trimethylamine N-oxide and the gut microbiota

Author

Hoyles, Lesley, primary, Jiménez-Pranteda, Maria L., additional, Chilloux, Julien, additional, Brial, Francois, additional, Myridakis, Antonis, additional, Aranias, Thomas, additional, Magnan, Christophe, additional, Gibson, Glenn R., additional, Sanderson, Jeremy D., additional, Nicholson, Jeremy K., additional, Gauguier, Dominique, additional, McCartney, Anne L., additional, and Dumas, Marc-Emmanuel, additional

Published
2017
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7. Lipid-rich diet enhances L-cell density in obese subjects and in mice through improved L-cell differentiation

Author

Aranias, Thomas, Grosfeld, Alexandra, Poitou, Christine, Omar, Amal Ait, Le Gall, Maude, Miquel, Sylvie, Garbin, Kevin, Ribeiro, Agnès, Bouillot, Jean-Luc, Bado, Andre, Brot-Laroche, Edith, Clément, Karine, Leturque, Armelle, Guilmeau, Sandra, Serradas, Patricia, Université Pierre et Marie Curie - Paris 6 (UPMC), Unité de Recherche sur les Maladies Cardiovasculaires, du Métabolisme et de la Nutrition = Research Unit on Cardiovascular and Metabolic Diseases (ICAN), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Institut de Cardiométabolisme et Nutrition = Institute of Cardiometabolism and Nutrition [CHU Pitié Salpêtrière] (IHU ICAN), CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Institut National de la Santé et de la Recherche Médicale (INSERM), Centre de recherche sur l'Inflammation (CRI (UMR_S_1149 / ERL_8252 / U1149)), Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Université Paris Descartes - Paris 5 (UPD5), MICrobiologie de l'ALImentation au Service de la Santé (MICALIS), Institut National de la Recherche Agronomique (INRA)-AgroParisTech, Hôpital Ambroise Paré [AP-HP], Université Pierre et Marie Curie - Paris 6 (UPMC)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU), Université Paris-Sorbonne (UP4), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Metabolisme et Differenciation Intestinale, Université Pierre et Marie Curie - Paris 6 (UPMC)-IFR58-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre de Recherche des Cordeliers (CRC), Université Pierre et Marie Curie - Paris 6 (UPMC)-École Pratique des Hautes Études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-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), ProdInra, Migration, Unité de Recherche sur les Maladies Cardiovasculaires, du Métabolisme et de la Nutrition = Institute of cardiometabolism and nutrition (ICAN), and Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [AP-HP]

Subjects
HFD, high-fat diet, endocrine system, ngn3, isl1, insulin gene enhancer protein-1, paired box protein-6, [SDV]Life Sciences [q-bio], neurogenin3, pax6, paired box protein-6, BrdU, bromodeoxyuridine, foxa1, forkhead box protein A1, PYY, peptide YY, peptide YY, BrdU, Enteroendocrine cells, GIP, PYY, digestive, oral, and skin physiology, GIP, glucose-dependent insulinotropic polypeptide, foxa2, GLP-1, glucagon-like peptide-1, foxa1, ngn3, neurogenin3, Gut hormones, foxa2, forkhead box protein A2, bromodeoxyuridine, CD, Intestine, [SDV] Life Sciences [q-bio], glucose-dependent insulinotropic polypeptide, forkhead box protein A1, High-fat diet, glucagon-like peptide-1, control diet, HFD, CD, control diet, isl1, GLP-1, insulin gene enhancer protein-1, pax6, hormones, hormone substitutes, and hormone antagonists, Research Article, forkhead box protein A2
Abstract

International audience; The enterohormone glucagon-like peptide-1 (GLP-1) is required to amplify glucose-induced insulin secretion that facilitates peripheral glucose utilisation. Alteration in GLP-1 secretion during obesity has been reported but is still controversial. Due to the high adaptability of intestinal cells to environmental changes, we hypothesised that the density of GLP-1-producing cells could be modified by nutritional factors to prevent the deterioration of metabolic condition in obesity. We quantified L-cell density in jejunum samples collected during Roux-en-Y gastric bypass in forty-nine severely obese subjects analysed according to their fat consumption. In mice, we deciphered the mechanisms by which a high-fat diet (HFD) makes an impact on enteroendocrine cell density and function. L-cell density in the jejunum was higher in obese subjects consuming >30 % fat compared with low fat eaters. Mice fed a HFD for 8 weeks displayed an increase in GLP-1-positive cells in the jejunum and colon accordingly to GLP-1 secretion. The regulation by the HFD appears specific to GLP-1-producing cells, as the number of PYY (peptide YY)-positive cells remained unchanged. Moreover, genetically obese ob/ob mice did not show alteration of GLP-1-positive cell density in the jejunum or colon, suggesting that obesity per se is not sufficient to trigger the mechanism. The higher L-cell density in HFD-fed mice involved a rise in L-cell terminal differentiation as witnessed by the increased expression of transcription factors downstream of neurogenin3 ( Ngn3 ). We suggest that the observed increase in GLP-1-positive cell density triggered by high fat consumption in humans and mice might favour insulin secretion and therefore constitute an adaptive response of the intestine to balance diet-induced insulin resistance.

Published
2015
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