Evaluation of low doses BPA-induced perturbation of glycemia by toxicogenomics points to a primary role of pancreatic islets and to the mechanism of toxicity

[1]  N. Chevalier,et al.  Endocrine disruptors: new players in the pathophysiology of type 2 diabetes? , 2015, Diabetes & metabolism.

[2]  Wenjun Xie,et al.  Calcium release channel RyR2 regulates insulin release and glucose homeostasis. , 2015, The Journal of clinical investigation.

[3]  Flavourings,et al.  Scientific Opinion on the risks to public health related to the presence of bisphenol A (BPA) in foodstuffs , 2015 .

[4]  C. Christophi,et al.  Preliminary evidence of the association between monochlorinated bisphenol A exposure and type II diabetes mellitus: A pilot study , 2015, Journal of environmental science and health. Part A, Toxic/hazardous substances & environmental engineering.

[5]  M. Ceccarelli,et al.  Cross-species toxicogenomic analyses and phenotypic anchoring in response to groundwater low-level pollution , 2014, BMC Genomics.

[6]  Qianyuan Li,et al.  Mitochondrion-mediated apoptosis is involved in reproductive damage caused by BPA in male rats. , 2014, Environmental toxicology and pharmacology.

[7]  C. Evans-Molina,et al.  Bisphenol A, obesity, and type 2 diabetes mellitus: genuine concern or unnecessary preoccupation? , 2014, Translational research : the journal of laboratory and clinical medicine.

[8]  M. Levy,et al.  Inflammatory Response in Islet Transplantation , 2014, International journal of endocrinology.

[9]  Andrew G Kirkley,et al.  Environmental Endocrine Disruption of Energy Metabolism and Cardiovascular Risk , 2014, Current Diabetes Reports.

[10]  X. Chen,et al.  Early-Life Exposure to Bisphenol A Induces Liver Injury in Rats Involvement of Mitochondria-Mediated Apoptosis , 2014, PloS one.

[11]  E. Jeung EFFECTS OF XENOESTROGENS ON STREPTOZOTOCIN-INDUCED DIABETIC MICE , 2014 .

[12]  Katarzyna A. Broniowska,et al.  Do β-Cells Generate Peroxynitrite in Response to Cytokine Treatment?* , 2013, The Journal of Biological Chemistry.

[13]  P. Marchetti,et al.  Exendin-4 protects pancreatic beta cells from palmitate-induced apoptosis by interfering with GPR40 and the MKK4/7 stress kinase signalling pathway , 2013, Diabetologia.

[14]  F. Brucker-Davis,et al.  Bisphenol A: an endocrine and metabolic disruptor. , 2013, Annales d'endocrinologie.

[15]  X. Chen,et al.  Hepatic DNA methylation modifications in early development of rats resulting from perinatal BPA exposure contribute to insulin resistance in adulthood , 2013, Diabetologia.

[16]  P. Bergsten,et al.  Functional differences between aggregated and dispersed insulin-producing cells , 2013, Diabetologia.

[17]  C. Ambrosino,et al.  Bisphenol A interferes with thyroid specific gene expression. , 2013, Toxicology.

[18]  L. Lind,et al.  Bisphenol A exposure increases liver fat in juvenile fructose-fed Fischer 344 rats. , 2013, Toxicology.

[19]  Y. Lin,et al.  Exposure to bisphenol A induces dysfunction of insulin secretion and apoptosis through the damage of mitochondria in rat insulinoma (INS-1) cells , 2013, Cell Death and Disease.

[20]  W. Xia,et al.  Low-level phenolic estrogen pollutants impair islet morphology and β-cell function in isolated rat islets. , 2012, The Journal of endocrinology.

[21]  Ning Li,et al.  Mitochondrial dysfunction in pancreatic β cells , 2012, Trends in Endocrinology & Metabolism.

[22]  L. Huc,et al.  Low concentrations of bisphenol A induce lipid accumulation mediated by the production of reactive oxygen species in the mitochondria of HepG2 cells. , 2012, Toxicology in vitro : an international journal published in association with BIBRA.

[23]  Paloma Alonso-Magdalena,et al.  Bisphenol-A acts as a potent estrogen via non-classical estrogen triggered pathways , 2012, Molecular and Cellular Endocrinology.

[24]  J. Gustafsson,et al.  Rapid Insulinotropic Action of Low Doses of Bisphenol-A on Mouse and Human Islets of Langerhans: Role of Estrogen Receptor β , 2012, PloS one.

[25]  Pascal G. P. Martin,et al.  Low doses of bisphenol a induce gene expression related to lipid synthesis and trigger triglyceride accumulation in adult mouse liver , 2012, Hepatology.

[26]  A. Shankar,et al.  Relationship between urinary bisphenol A levels and diabetes mellitus. , 2011, The Journal of clinical endocrinology and metabolism.

[27]  R. Curi,et al.  Regulation of insulin secretion and reactive oxygen species production by free fatty acids in pancreatic islets , 2011, Islets.

[28]  Naoki Kiyosawa,et al.  Practical Application of Toxicogenomics for Profiling Toxicant-Induced Biological Perturbations , 2010, International journal of molecular sciences.

[29]  P. Kovacic How safe is bisphenol A? Fundamentals of toxicity: metabolism, electron transfer and oxidative stress. , 2010, Medical hypotheses.

[30]  I. Quesada,et al.  Bisphenol A Exposure during Pregnancy Disrupts Glucose Homeostasis in Mothers and Adult Male Offspring , 2010, Environmental health perspectives.

[31]  Paloma Alonso-Magdalena,et al.  Bisphenol-A: a new diabetogenic factor? , 2010, Hormones.

[32]  D. Tosh,et al.  Isolation and culture of adult mouse hepatocytes. , 2010, Methods in molecular biology.

[33]  J. Shaw,et al.  Global estimates of the prevalence of diabetes for 2010 and 2030. , 2010, Diabetes research and clinical practice.

[34]  K. Korach,et al.  Importance of Extranuclear Estrogen Receptor-α and Membrane G Protein–Coupled Estrogen Receptor in Pancreatic Islet Survival , 2009, Diabetes.

[35]  I. Quesada,et al.  The pancreatic β-cell as a target of estrogens and xenoestrogens: Implications for blood glucose homeostasis and diabetes , 2009, Molecular and Cellular Endocrinology.

[36]  I. Quesada,et al.  The role of estrogen receptors in the control of energy and glucose homeostasis , 2008, Steroids.

[37]  E. Stefani,et al.  Pancreatic Insulin Content Regulation by the Estrogen Receptor ERα , 2008, PloS one.

[38]  C. Ripoll,et al.  Bisphenol-A disruption of the endocrine pancreas and blood glucose homeostasis. , 2008, International journal of andrology.

[39]  Antonia M. Calafat,et al.  Exposure of the U.S. Population to Bisphenol A and 4-tertiary-Octylphenol: 2003–2004 , 2007, Environmental health perspectives.

[40]  J. Vílchez,et al.  Bisphenol-A and chlorinated derivatives in adipose tissue of women. , 2007, Reproductive toxicology.

[41]  Laura N. Vandenberg,et al.  Human exposure to bisphenol A (BPA). , 2007, Reproductive toxicology.

[42]  Dolca Thomas,et al.  Mitochondrial targeting with antioxidant peptide SS-31 prevents mitochondrial depolarization, reduces islet cell apoptosis, increases islet cell yield, and improves posttransplantation function. , 2007, Journal of the American Society of Nephrology : JASN.

[43]  G. Mortier,et al.  qBase relative quantification framework and software for management and automated analysis of real-time quantitative PCR data , 2007, Genome Biology.

[44]  William Hagopian,et al.  Environmental factors in the development of Type 1 diabetes , 2007, Reviews in Endocrine and Metabolic Disorders.

[45]  S. Legrand-Poels,et al.  NF-κB activation by reactive oxygen species: Fifteen years later , 2006 .

[46]  J. Ruderman Faculty Opinions recommendation of The estrogenic effect of bisphenol A disrupts pancreatic beta-cell function in vivo and induces insulin resistance. , 2006 .

[47]  Glen R. Boyd,et al.  Endocrine Disrupting Chemicals Research Program of the U.S. Environmental Protection Agency: Summary of a Peer-Review Report , 2006, Environmental health perspectives.

[48]  Paloma Alonso-Magdalena,et al.  The Estrogenic Effect of Bisphenol A Disrupts Pancreatic β-Cell Function In Vivo and Induces Insulin Resistance , 2005, Environmental health perspectives.

[49]  S. Legrand-Poels,et al.  NF-kappaB activation by reactive oxygen species: fifteen years later. , 2006, Biochemical pharmacology.

[50]  Nils Welsh,et al.  Mechanisms of pancreatic beta-cell death in type 1 and type 2 diabetes: many differences, few similarities. , 2005, Diabetes.

[51]  Thomas Werner,et al.  MatInspector and beyond: promoter analysis based on transcription factor binding sites , 2005, Bioinform..

[52]  P. Mathur,et al.  Bisphenol A induces reactive oxygen species generation in the liver of male rats. , 2003, Toxicology.

[53]  T. Speed,et al.  Summaries of Affymetrix GeneChip probe level data. , 2003, Nucleic acids research.

[54]  B. Soria,et al.  Low doses of the endocrine disruptor Bisphenol‐A and the native hormone 17β‐estradiol rapidly activate the transcription factor CREB , 2002, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[55]  Lee Bennett,et al.  Prediction of compound signature using high density gene expression profiling. , 2002, Toxicological sciences : an official journal of the Society of Toxicology.

[56]  G. Melino,et al.  High glucose causes apoptosis in cultured human pancreatic islets of Langerhans: a potential role for regulation of specific Bcl family genes toward an apoptotic cell death program. , 2001, Diabetes.

[57]  S Z Cagen,et al.  The relative bioavailability and metabolism of bisphenol A in rats is dependent upon the route of administration. , 2000, Toxicological sciences : an official journal of the Society of Toxicology.

[58]  H. Jinno,et al.  Suppression of male-specific cytochrome P450 isoforms by bisphenol A in rat liver , 1998, Archives of Toxicology.

[59]  C. Florentz,et al.  Isoleucylation properties of native human mitochondrial tRNAIle and tRNAIle transcripts. Implications for cardiomyopathy-related point mutations (4269, 4317) in the tRNAIle gene. , 1998, Human molecular genetics.

[60]  T. Pozzan,et al.  Mitochondrial activation directly triggers the exocytosis of insulin in permeabilized pancreatic β‐cells , 1997, The EMBO journal.

[61]  T. Maki,et al.  MINIMUM NUMBER OF ISLETS REQUIRED TO MAINTAIN EUGLYCEMIA AND THEIR REDUCED IMMUNOGENICITY AFTER TRANSPLANTATION INTO DIABETIC MICE , 1993, Transplantation.

[62]  W C Greene,et al.  NF-kappa B controls expression of inhibitor I kappa B alpha: evidence for an inducible autoregulatory pathway. , 1993, Science.