Effects of bisphenol A on metabolism and evidences of a mode of action mediated through endocrine disruption. (5th November 2018)

• Record Type: Journal Article
• Authors: Le Magueresse-Battistoni, Brigitte; Multigner, Luc; Beausoleil, Claire; Rousselle, Christophe
• Is Part Of: Molecular and cellular endocrinology. Volume 475(2018)
• Page Start: 74
• Page End: 91
• Publication Date: 2018-11-05
• Subjects: Bisphenol A -- BPA -- Endocrine disruption -- Obesity -- Type 2 diabetes -- Insulin; BAT brown adipose tissue -- BMI body mass index -- bw body weight -- DES diethylstilbestrol -- DM Diabete mellitus -- ED endocrine disruptor -- eGFR estimated glomerular filtration -- ERR estrogen related receptor -- ERRγ or ERRgamma Estrogen-related receptor gamma -- Erα or ERalpha estrogen receptor α -- ERβ or ERbeta estrogen receptor beta -- FABP4 fatty acid binding protein 4 -- GD gestation day -- GLUT4 Glucose transporter type 4 -- GPER or GPR30 G protein-coupled estrogen receptor or G protein-coupled receptor 30, the membranous form of estrogen receptor -- GR glucocorticoid receptor (NR3C1) -- GSH Glutathione -- GSIS Glucose-Stimulated Insulin Secretion -- GTT glucose tolerance test -- HFD High Fat Diet -- IAPP Islet Amyloid PolyPeptide -- ipGTT intraperitoneal glucose tolerance tests -- ipITT intraperitoneal insulin tolerance tests -- IR insulin receptor -- IRS-1 insulin receptor substrate 1 -- IS insulin sensitivity -- MDI induction medium containing methylisobutylxanthine, dexamethasone, insulin, used in protocols to induce differentiation of 3T3-L1 cells into adipocyte-like cells -- MoA mode of action -- MSCs Mesenchymal Stromal Cells -- NEFA Non-Esterified Fatty Acids -- NHANES US National Health and Nutrition Examination Survey -- NHS nurses' health study -- NHSII nurses' health study II -- PI3K phosphoinositide 3-kinase -- PND postnatal day -- PPARγ Peroxisome Proliferator Activated Receptor gamma -- PPRE PPARγ Response Element -- ROSI Rosiglitazone -- SOD superoxide dismutase -- TBT Tributyltin -- TD2M Type-2 diabetes mellitus -- TDI tolerable daily intake -- TG triglyceride -- TO T0070907, used as a PPARγ antagonist -- WAT White Adipose Tissue -- WB Western blot; Endocrinology -- Periodicals; Molecular biology -- Periodicals; Cytology -- Periodicals; Endocrinology -- Periodicals; Hormones -- Periodicals; Endocrinologie -- Périodiques; Cytology; Endocrinology; Molecular biology; Periodicals; 573.4
• DOI: 10.1016/j.mce.2018.02.009
• Languages: English
• ISSNs: 0303-7207

Abstract

Abstract: Based on rodent studies after prenatal and/or perinatal or adult exposure, there is now evidence that BPA may increase metabolic disturbances eventually leading to type-2 diabetes development via an ED MoA. In particular, BPA has been shown to alter insulin synthesis and/or release by pancreatic β-cells, and insulin signaling within insulin-sensitive organs (i.e., liver, muscle, adipose tissues). This resulted in variations in the expression of specific hepatic or adipose tissue markers, which are indicative of a state of insulin resistance. These effects are considered by experts to be hallmarks of adverse hormonal effects, each leading to insulin resistance within the different insulin-sensitive tissues. Although epidemiological studies are inconclusive, these effects are considered relevant for humans, because similarities exist in homeostatic regulation of insulin production and sensitivity between rodents and humans and because evidence was also shown through in vitro experimental data using human cells or tissues. Highlights: BPA decreases insulin synthesis and secretion, after prenatal or adult exposure. BPA decreases insulin action, after prenatal, perinatal and adult exposure. There is good evidence of BPA toxicity on pancreatic β -cells. Estrogen receptor mechanism (β/α or GPR30 types) may be involved. Epigenetic mechanisms are also suggested.