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| 1 | Endocrine disrupting chemicals in mixture and obesity,diabetes and related metabolic disorders显示文摘Obesity and associated metabolic disorders represent a major societal challenge in health and quality of life with large psychological consequences in addition to physical disabilities. They are also one of the leading causes of morbidity and mortality. Although, different etiologic factors including excessive food intake and reduced physical activity have been well identified, they cannot explain the kinetics of epidemic evolution of obesity and diabetes with prevalence rates reaching pandemic proportions. Interestingly, convincing data have shown that environmental pollutants, specifically those endowed with endocrine disrupting activities, could contribute to the etiology of these multifactorial metabolic disorders. Within this review, we will recapitulate characteristics of endocrine disruption. We will demonstrate that metabolic disorders could originate from endocrine disruption with a particular focus on convincing data from the literature. Eventually, we will present how handling an original mouse model of chronic exposition to a mixture of pollutants allowed demonstrating that a mixture of pollutants each at doses beyond their active dose could induce substantial deleterious effects on several metabolic end-points. This proof-of-concept study, as well as other studies on mixtures of pollutants, stresses the needs for revisiting the current threshold model used in risk assessment which does not take into account potential effects of mixtures containing pollutants at environmental doses, e.g., the real life exposure. Certainly, more studies are necessary to better determine the nature of the chemicals to which humans are exposed and at which level, and their health impact. As well, research studies on substitute products are essential to identify harmless molecules. | Brigitte Le Magueresse-Battistoni Emmanuel Labaronne Hubert Vidal Danielle Naville | 2017 | World Journal of Biological Chemistry2017，8，2： | 4 |
| 2 | Dual Peroxisome Proliferator–Activated Receptor α/δ Agonist GFT505 Improves Hepatic and Peripheral Insulin Sensitivity in Abdominally Obese Subjects显示文摘 | Bertrand Cariou Rémy Hanf Stéphanie Lambert-Porcheron Yassine Za?r Valérie Sauvinet Benoit No?l Laurent Flet Hubert Vidal Bart Staels Martine Laville | 2013 | Diabetes Care2013，，10： | 2 |
| 3 | Mitochondria-associated endoplasmic reticulum membranes allow adaptation of mitochondrial metabolism to glucose availability in the liver显示文摘Mitochondria-associated endoplasmic reticulum membranes(MAM)play a key role in mitochondrial dynamics and function and in hepatic insulin action.Whereas mitochondria are important regulators of energy metabolism,the nutritional regulation of MAM in the liver and its role in the adaptation of mitochondria physiology to nutrient availability are unknown.In this study,we found that the fasted to postprandial transition reduced the number of endoplasmic reticulum-mitochondria contact points in mouse liver.Screening of potential hormonal/metabolic signals revealed glucose as the main nutritional regulator of hepatic MAM integrity both in vitro and in vivo.Glucose reduced organelle interactions through the pentose phosphate-protein phosphatase 2A(PP-PP2A)pathway,induced mitochondria fission,and impaired respiration.Blocking MAM reduction counteracted glucose-induced mitochondrial alterations.Furthermore,disruption of MAM integrity mimicked effects of glucose on mitochondria dynamics and function.This glucose-sensing system is deficient in the liver of insulin-resistant ob/ob and cyclophilin D-KO mice,both characterized by chronic disruption of MAM integrity,mitochondrial fission,and altered mitochondrial respiration.These data indicate that MAM contribute to the hepatic glucose-sensing system,allowing regulation of mitochondria dynamics and function during nutritional transition.Chronic disruption of MAM may participate in hepatic mitochondrial dysfunction associated with insulin resistance. | Pierre Theurey Emily Tubbs Guillaume Vial Julien Jacquemetton Nadia Bendridi Marie-Agnes Chauvin Muhammad Rizwan Alam Muriel Le Romancer Hubert Vidal Jennifer Rieusset | 2016 | Journal of Molecular Cell Biology2016，8，2： | 2 |
| 4 | Nutritionally Induced Changes in the Peroxisome Proliferator-Activated Receptor-α Gene Expression in Liver of Suckling Rats Are Dependent on Insulinaemia显示文摘 | Maribel Panadero Hubert Vidal Emilio Herrera Carlos Bocos | 2001 | Archives of Biochemistry and Biophysics2001，，2： | 1 |
| 5 | Alterations of insulin signaling in type 2 diabetes:A review of the current evidence from humans显示文摘 | Sara Frojdo Hubert Vidal Luciano Pirola | 2009 | Biochimica et Biophysica Acta (BBA)-Molecular Basis of Disease2009，1792，2： | 1 |
| 6 | Mitochondrial dysfunction results from oxidative stress in the skeletal muscle of diet-induced insulin-resistant mice显示文摘 | Bonnard Charlotte Durand Annie Peyrol Simone Chanseaume Emilie Chauvin Marie-Agnes Morio Béatrice Vidal Hubert Rieusset Jennifer | 2008 | Journal of Clinical Investigation2008，，2： | 1 |
| 7 | Plasma acylation stimulating protein concentration and subcutaneous adipose tissue C3 mRNA expression in nondiabetic and type 2 diabetic men显示文摘 | Koistinen Hubert Vidal | 2001 | Arterioscler Thromb Vasc Biol2001，21，： | 1 |
| 8 | Protein acetylation mechanisms in the regulation of insulin and insulin-like growth factor 1 signalling显示文摘 | Luciano Pirola Ouafa Zerzaihi Hubert Vidal Florence Solari | 2012 | Molecular and Cellular Endocrinology (-)2012，，1： | 1 |
| 9 | Involvement of glycated albumin in adipose-derived-stem cellmediated interleukin 17 secreting T helper cell activation显示文摘BACKGROUND Advanced glycation end products(AGE)are a marker of various diseases including diabetes,in which they participate to vascular damages such as retinopathy,nephropathy and coronaropathy.Besides those vascular complications,AGE are involved in altered metabolism in many tissues,including adipose tissue(AT)where they contribute to reduced glucose uptake and attenuation of insulin sensitivity.AGE are known to contribute to type 1 diabetes(T1D)through promotion of interleukin(IL)-17 secreting T helper(Th17)cells.AIM To investigate whether lean adipose-derived stem cells(ASC)could be able to induce IL-17A secretion,with the help of AGE.METHODS As we have recently demonstrated that ASC are involved in Th17 cell promotion when they are harvested from obese AT,we used the same co-culture model to measure the impact of glycated human serum albumin(G-HSA)on human lean ASC interacting with blood mononuclear cells.IL-17A and pro-inflammatory cytokine secretion were measured by ELISA.Receptor of AGE(RAGE)together with intercellular adhesion molecule 1(ICAM-1),human leukocyte Antigen(HLA)-DR,cluster of differentiation(CD)41,and CD62P surface expressions were measured by cytofluorometry.Anti-RAGE specific monoclonal antibody was added to co-cultures in order to evaluate the role of RAGE in IL-17A production.RESULTS Results showed that whereas 1%G-HSA only weakly potentiated the production of IL-17A by T cells interacting with ASC harvested from obese subjects,it markedly increased IL-17A,but also interferon gamma and tumor necrosis factor alpha production in the presence of ASC harvested from lean individuals.This was associated with increased expression of RAGE and HLA-DR molecule by cocultured cells.Moreover,RAGE blockade experiments demonstrated RAGE specific involvement in lean ASC-mediated Th-17 cell activation.Finally,platelet aggregation and ICAM-1,which are known to be induced by AGE,were not involved in these processes.CONCLUSION Thus,our results demonstrated that G-HSA potentiated lean ASC-mediated IL-17A production in AT,suggesting a new mechanism by which AGE could contribute to T1D pathophysiology. | Julien Pestel Maud Robert Sara Corbin Hubert Vidal Assia Eljaafari | 2020 | World Journal of Stem Cells2020，12，7： | 0 |
| 10 | Repsol石油公司园区显示文摘 | Jesús Román Concha Pe a Marcus Lassan Carolina Fernández Conchi Cobo Guillermo Vidal Bodo Schumacher Laura Díaz Hubert Lionnez María Millán Hugo Berenguer Guillermo Cervantes Beatriz Heras Zaloa Mayor María Martínez Miguel García Irene Zurdo María Iglesias Alfonso Quiroga 刘亦师 | 2014 | 建筑学报2014，，4： | 0 |
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