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165 results on '"Tordjman J"'

16. Noninvasive diagnosis of nonalcoholic steatohepatitis disease based on clinical decision support system

Author

Douali, N., Abdennour, M., Sasso, M., Miette, V., Tordjman, J., Bedossa, P., Veyrie, N., Poitou, C., Aron-Wisnewsky, J., Clément, K., Jaulent, M.C., Zucker, Jean-Daniel, Lehmann, C.U. (ed.), Ammenwerth, E. (ed.), and Nøhr, C. (ed.)

Subjects
nutritional and metabolic diseases, digestive system, digestive system diseases
Abstract

Non-alcoholic fatty liver disease (NAFLD) is a hepatic dis-ease associated with metabolic syndrome. NAFLD covers a spectrum of liver disease from steatosis to non-alcoholic stea-tohepatitis (NASH) and cirrhosis. NASH is a disease evolving under the influence of various stimuli still poorly understood. In this paper we present new clinical decision support system (CDSS) for the diagnosis of NASH and the comparison of this system with machine learn-ing algorithms.

Published
2013

17. Évaluation prospective de la graisse toxique péri-rénale au cours des néphrectomies partielles – rôle prédictif des caractéristiques clinico-radiologiques sur les résultats postopératoires et analyse histologique

Author

Dariane, C., primary, Badoual, C., additional, Tordjman, J., additional, Clément, K., additional, Le Guilchet, T., additional, Hurel, S., additional, Pietak, M., additional, Méjean, A., additional, and Timsit, M., additional

Published
2015
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23. Fibrosis in human adipose tissue : composition, distribution, and link with lipid metabolism and fat mass loss [plus Appendix : Experimental procedures and results]

Author

Divoux, A., Tordjman, J., Lacasa, D., Veyrie, N., Hugol, D., Aissat, A., Basdevant, A., Guerre-Millo, M., Poitou, C., Zucker, Jean-Daniel, Bedossa, P., Clément, K., Unité de modélisation mathématique et informatique des systèmes complexes [Bondy] (UMMISCO), and Institut de Recherche pour le Développement (IRD [France-Nord])-Institut de la francophonie pour l'informatique-Université Cheikh Anta Diop [Dakar, Sénégal] (UCAD)-Université Gaston Bergé (Saint-Louis, Sénégal)-Université Cadi Ayyad [Marrakech] (UCA)-Université de Yaoundé I-Sorbonne Université (SU)

Subjects
FRANCE, [SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism, [SDV.AEN]Life Sciences [q-bio]/Food and Nutrition, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
Abstract

Objective : Fibrosis is a newly appreciated hallmark of the pathological alteration of human white adipose tissue (WAT). We investigated the composition of subcutaneous (scWAT) and omental WAT (oWAT) fibrosis in obesity and its relationship with metabolic alterations and surgery-induced weight loss. Research design and methods : Surgical biopsies for scWAT and oWAT were obtained in 65 obese (BMI 48.2 ± 0.8 kg/m(2)) and 9 lean subjects (BMI 22.8 ± 0.7 kg/m(2)). Obese subjects who were candidates for bariatric surgery were clinically characterized before, 3, 6, and 12 months after surgery, including fat mass evaluation by dual energy X-ray absorptiometry. WAT fibrosis was quantified and characterized using quantitative PCR, microscopic observation, and immunohistochemistry. Results : Fibrosis amount, distribution and collagen types (I, III, and VI) present distinct characteristics in lean and obese subjects and with WAT depots localization (subcutaneous or omental). Obese subjects had more total fibrosis in oWAT and had more pericellular fibrosis around adipocytes than lean subjects in both depots. Macrophages and mastocytes were highly represented in fibrotic bundles in oWAT, whereas scWAT was more frequently characterized by hypocellular fibrosis. The oWAT fibrosis negatively correlated with omental adipocyte diameters (R = -0.30, P = 0.02), and with triglyceride levels (R = -0.42, P < 0.01), and positively with apoA1 (R = 0.25, P = 0.05). Importantly, scWAT fibrosis correlated negatively with fat mass loss measured at the three time points after surgery. Conclusions : Our data suggest differential clinical consequences of fibrosis in human WAT. In oWAT, fibrosis could contribute to limit adipocyte hypertrophy and is associated with a better lipid profile, whereas scWAT fibrosis may hamper fat mass loss induced by surgery.

Published
2010
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26. Macrophage Gene Expression in Adipose Tissue is Associated with Insulin Sensitivity and Serum Lipid Levels Independent of Obesity

Author

Ahlin, S., primary, Sjöholm, K., additional, Jacobson, P., additional, Andersson-Assarsson, J.C., additional, Walley, A., additional, Tordjman, J., additional, Poitou, C., additional, Prifti, E., additional, Jansson, P.-A., additional, Borén, J., additional, Sjöström, L., additional, Froguel, P., additional, Bergman, R.N., additional, Carlsson, L.M.S., additional, Olsson, B., additional, and Svensson, P.-A., additional

Published
2013
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27. 104 A CANDIDATE-GENE APPROACH TO VALIDATION OF GENETIC MODIFIER ASSOCIATIONS USING A LARGE COHORT WITH HISTOLOGICALLY CHARACTERISED NON-ALCOHOLIC FATTY LIVER DISEASE

Author

Anstee, Q.M., primary, Darlay, R., additional, Leathart, J., additional, Liu, Y.-L., additional, Tordjman, J., additional, Clement, K., additional, Aithal, G., additional, Valenti, L., additional, Van Gaal, L., additional, Stickel, F., additional, Alison, M., additional, Romero-Gomez, M., additional, Andrade, R., additional, Reeves, H., additional, Bedossa, P., additional, Pihlajamaki, J., additional, Kotronen, A., additional, Yki-Jarvinen, H., additional, Chalasani, N., additional, Kleiner, D.E., additional, Rotter, J., additional, Burt, A., additional, Ratziu, V., additional, Cordell, H.J., additional, Daly, A.K., additional, and Day, C.P., additional

Published
2013
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28. P2157 Altérations de l’immunité intestinale dans l’obésité humaine

Author

Sepulveda, M.M., primary, André, S., additional, Cotillard, A., additional, Ting, H.F., additional, Remark, R., additional, Tordjman, J., additional, Veyrie, N., additional, Genser, L., additional, Leturque, A., additional, Poitou, C., additional, Fridman, C.S., additional, Clément, K., additional, and Brot-Laroche, E., additional

Published
2013
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29. P2161 Quelles sont les conséquences d’un régime riche en graisse sur les cellules entéroendocrines ?

Author

Aranias, T., primary, Grosfeld, A., additional, Cotillard, A., additional, Omar, A.A., additional, Tordjman, J., additional, Le Gall, M., additional, Benkouhi, A., additional, Garbin, K., additional, Lacorte, J.-M., additional, Brot-Laroche, E., additional, Clément, K., additional, Leturque, A., additional, Poitou, C., additional, Guilmeau, S., additional, and Serradas, P., additional

Published
2013
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31. Obesity-Dependent Metabolic Signatures Associated with Nonalcoholic Fatty Liver Disease Progression

Author

Barr, J., primary, Caballería, J., additional, Martínez-Arranz, I., additional, Domínguez-Díez, A., additional, Alonso, C., additional, Muntané, J., additional, Pérez-Cormenzana, M., additional, García-Monzón, C., additional, Mayo, R., additional, Martín-Duce, A., additional, Romero-Gómez, M., additional, Iacono, O. Lo, additional, Tordjman, J., additional, Andrade, R. J., additional, Pérez-Carreras, M., additional, Marchand-Brustel, Y. Le, additional, Tran, A., additional, Fernández-Escalante, C., additional, Arévalo, E., additional, García-Unzueta, M., additional, Clement, K., additional, Crespo, J., additional, Gual, P., additional, Gómez-Fleitas, M., additional, Martínez-Chantar, M. L., additional, Castro, A., additional, Lu, S. C., additional, Vázquez-Chantada, M., additional, and Mato, J. M., additional

Published
2012
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35. 696 ELEVATED EXPRESSION OF OSTEOPONTIN IS RELATED TO ADIPOSE TISSUE MACROPHAGE ACCUMULATION AND LIVER STEATOSIS IN MORBID OBESITY

Author

Bertola, A., primary, Deveaux, V., additional, Bonnafous, S., additional, Rousseau, D., additional, Anty, R., additional, Wakkach, A., additional, Dahman, M., additional, Tordjman, J., additional, Clément, K., additional, McQuaid, S.E., additional, Frayn, K.N., additional, Huet, P.M., additional, Gugenheim, J., additional, Lotersztajn, S., additional, Le Marchand-Brustel, Y., additional, Tran, A., additional, and Gual, P., additional

Published
2009
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36. P221 L’élévation de l’expression de l’ostéopontine dans l’obésité morbide est corrélée à l’accumulation des macrophages dans le tissu adipeux et à la stéatose hépatique

Author

Bertola, A., primary, Deveaux, V., additional, Bonnafous, S., additional, Rousseau, D., additional, Anty, R., additional, Dahman, M., additional, Tordjman, J., additional, Clément, K., additional, Lotersztajn, S., additional, Le Marchand-Brustel, Y., additional, Tran, A., additional, and Gual, P., additional

Published
2009
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41. Obesity-Dependent MetabolicSignatures Associated with Nonalcoholic Fatty Liver Disease Progression.

Author

Barr, J., Caballería, J., Martínez-Arranz, I., Domínguez-Díez, A., Alonso, C., Muntané, J., Pérez-Cormenzana, M., García-Monzón, C., Mayo, R., Martín-Duce, A., Romero-Gómez, M., Iacono, O. Lo, Tordjman, J., Andrade, R. J., Pérez-Carreras, M., Marchand-Brustel, Y. Le, Tran, A., Fernández-Escalante, C., Arévalo, E., and García-Unzueta, M.

Published
2012
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42. GLUT2 accumulation in enterocyte apical and intracellular membranes: a study in morbidly obese human subjects and ob/ob and high fat-fed mice.

Author

Ait-Omar A, Monteiro-Sepulveda M, Poitou C, Le Gall M, Cotillard A, Gilet J, Garbin K, Houllier A, Château D, Lacombe A, Veyrie N, Hugol D, Tordjman J, Magnan C, Serradas P, Clément K, Leturque A, Brot-Laroche E, Ait-Omar, Amal, and Monteiro-Sepulveda, Milena

Subjects
HYPOGLYCEMIC agents, METFORMIN, ANIMAL experimentation, ANIMALS, CELL membranes, EPITHELIAL cells, CARBOHYDRATE content of food, FAT content of food, MICE, TYPE 2 diabetes, MORBID obesity
Abstract

Objective: In healthy rodents, intestinal sugar absorption in response to sugar-rich meals and insulin is regulated by GLUT2 in enterocyte plasma membranes. Loss of insulin action maintains apical GLUT2 location. In human enterocytes, apical GLUT2 location has not been reported but may be revealed under conditions of insulin resistance.Research Design and Methods: Subcellular location of GLUT2 in jejunal enterocytes was analyzed by confocal and electron microscopy imaging and Western blot in 62 well-phenotyped morbidly obese subjects and 7 lean human subjects. GLUT2 locations were assayed in ob/ob and ob/+ mice receiving oral metformin or in high-fat low-carbohydrate diet-fed C57Bl/6 mice. Glucose absorption and secretion were respectively estimated by oral glucose tolerance test and secretion of [U-(14)C]-3-O-methyl glucose into lumen.Results: In human enterocytes, GLUT2 was consistently located in basolateral membranes. Apical GLUT2 location was absent in lean subjects but was observed in 76% of obese subjects and correlated with insulin resistance and glycemia. In addition, intracellular accumulation of GLUT2 with early endosome antigen 1 (EEA1) was associated with reduced MGAT4a activity (glycosylation) in 39% of obese subjects on a low-carbohydrate/high-fat diet. Mice on a low-carbohydrate/high-fat diet for 12 months also exhibited endosomal GLUT2 accumulation and reduced glucose absorption. In ob/ob mice, metformin promoted apical GLUT2 and improved glucose homeostasis. Apical GLUT2 in fasting hyperglycemic ob/ob mice tripled glucose release into intestinal lumen.Conclusions: In morbidly obese insulin-resistant subjects, GLUT2 was accumulated in apical and/or endosomal membranes of enterocytes. Functionally, apical GLUT2 favored and endosomal GLUT2 reduced glucose transepithelial exchanges. Thus, altered GLUT2 locations in enterocytes are a sign of intestinal adaptations to human metabolic pathology. [ABSTRACT FROM AUTHOR]

Published
2011
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50. Tumor suppressor role of cytoplasmic polyadenylation element binding protein 2 (CPEB2) in human mammary epithelial cells.

Author

Tordjman J, Majumder M, Amiri M, Hasan A, Hess D, and Lala PK

Subjects
Animals, CRISPR-Cas Systems, Cell Movement, Cell Proliferation, Cyclooxygenase 2 metabolism, Epithelial Cells metabolism, Epithelial-Mesenchymal Transition, Female, Gene Knockout Techniques, Heterografts, Humans, MCF-7 Cells, Mice, Mice, Inbred NOD, Mice, SCID, MicroRNAs metabolism, Protein Isoforms, RNA, Small Interfering metabolism, RNA-Binding Proteins genetics, Tumor Suppressor Protein p53 metabolism, Breast cytology, Breast Neoplasms pathology, RNA-Binding Proteins metabolism
Abstract

Background: Over-expression of cyclooxygenase (COX)-2 promotes breast cancer progression by multiple mechanisms, including induction of stem-like cells (SLC). Combined gene expression and microRNA microarray analyses of empty vector vs COX-2- transfected COX-2 low MCF7 breast cancer cell line identified two COX-2-upregulated microRNAs, miR-526b and miR-655, both found to be oncogenic and SLC-promoting. Cytoplasmic Polyadenylation Element-Binding Protein 2 (CPEB2) was the single common target of both microRNAs, the functions of which remain controversial. CPEB2 has multiple isoforms (A-F), and paradoxically, a high B/A ratio was reported to impart anoikis-resistance and metastatic phenotype in triple- negative breast cancer cells. We tested whether CPEB2 is a tumor suppressor in mammary epithelial cells., Methods: We knocked-out CPEB2 in the non-tumorigenic mammary epithelial cell line MCF10A by CRISPR/Cas9-double nickase approach, and knocked-down CPEB2 with siRNAs in the poorly malignant MCF7 cell line, both lines being high CPEB2-expressing. The resultant phenotypes for oncogenity were tested in vitro for both lines and in vivo for CPEB2KO cells. Finally, CPEB2 expression was compared between human breast cancer and non-tumor breast tissues., Results: CPEB2 (isoform A) expression was inversely correlated with COX-2 or the above microRNAs in COX-2-divergent breast cancer cell lines. CPEB2KO MCF10A cells exhibited oncogenic properties including increased proliferation, migration, invasion, EMT (decreased E-Cadherin, increased Vimentin, N-Cadherin, SNAI1, and ZEB1) and SLC phenotype (increased tumorsphere formation and SLC marker-expression). Tumor-suppressor p53 protein was shown to be a novel translationally-regulated target of CPEB2, validated with polysome profiling. CPEB2KO, but not wild-type cells produced lung colonies upon intravenous injection and subcutaneous tumors and spontaneous lung metastases upon implantation at mammary sites in NOD/SCID/IL2Rϒ-null mice, identified with HLA immunostaining. Similarly, siRNA-mediated CPEB2 knockdown in MCF7 cells promoted oncogenic properties in vitro. Human breast cancer tissues (n = 105) revealed a lower mRNA expression for CPEB2 isoform A and also a lower A/B isoform ratio than in non-tumour breast tissues (n = 20), suggesting that CPEB2A accounts for the tumor-suppressor functions of CPEB2., Conclusions: CPEB2, presumably the isoform A, plays a key role in suppressing tumorigenesis in mammary epithelial cells by repressing EMT, migration, invasion, proliferation and SLC phenotype, via multiple targets, including a newly-identified translational target p53.

Published
2019
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