[1] BJÖRNSDOTTER M K, de BOER J, BALLESTEROS-GÓMEZ A. Bisphenol A and replacements in thermal paper: A review[J]. Chemosphere, 2017, 182: 691-706. doi: 10.1016/j.chemosphere.2017.05.070
[2] ROCHESTER J R. Bisphenol A and human health: A review of the literature[J]. Reproductive Toxicology, 2013, 42: 132-155. doi: 10.1016/j.reprotox.2013.08.008
[3] GEENS T, AERTS D, BERTHOT C, et al. A review of dietary and non-dietary exposure to bisphenol-A[J]. Food and Chemical Toxicology, 2012, 50(10): 3725-3740. doi: 10.1016/j.fct.2012.07.059
[4] VANDENBERG L N, HAUSER R, MARCUS M, et al. Human exposure to bisphenol A (BPA)[J]. Reproductive Toxicology, 2007, 24(2): 139-177. doi: 10.1016/j.reprotox.2007.07.010
[5] YANG M, KIM S Y, LEE S M, et al. Biological monitoring of bisphenol A in a Korean population[J]. Archives of Environmental Contamination and Toxicology, 2003, 44(4): 546-551. doi: 10.1007/s00244-002-2124-0
[6] ROTIMI O A, OLAWOLE T D, de CAMPOS O C, et al. Bisphenol A in Africa: A review of environmental and biological levels[J]. Science of the Total Environment, 2021, 764: 142854. doi: 10.1016/j.scitotenv.2020.142854
[7] 王盈灿, 沈理笑, 陈瑶, 等. 上海市学龄儿童双酚A暴露现状及与肥胖关系的初步研究[J]. 中国儿童保健杂志, 2015, 23(4): 344-347. doi: 10.11852/zgetbjzz2015-23-04-03 WANG Y C, SHEN L X, CHEN Y, et al. Preliminary study of school-age children exposure to bisphenol-A and its relationship with obesity in Shanghai[J]. Chinese Journal of Child Health Care, 2015, 23(4): 344-347 (in Chinese). doi: 10.11852/zgetbjzz2015-23-04-03
[8] VANDENBERG L N, CHAHOUD I, HEINDEL J J, et al. Urinary, circulating, and tissue biomonitoring studies indicate widespread exposure to bisphenol A[J]. Environmental Health Perspectives, 2010, 118(8): 1055-1070. doi: 10.1289/ehp.0901716
[9] LI D K, ZHOU Z J, MIAO M H, et al. Urine bisphenol-A (BPA) level in relation to Semen quality[J]. Fertility and Sterility, 2011, 95(2): 625-630. e4.
[10] PERERA F, VISHNEVETSKY J, HERBSTMAN J B, et al. Prenatal bisphenol a exposure and child behavior in an inner-city cohort[J]. Environmental Health Perspectives, 2012, 120(8): 1190-1194. doi: 10.1289/ehp.1104492
[11] PELCH K, WIGNALL J A, GOLDSTONE A E, et al. A scoping review of the health and toxicological activity of bisphenol A (BPA) structural analogues and functional alternatives[J]. Toxicology, 2019, 424: 152235. doi: 10.1016/j.tox.2019.06.006
[12] KONNO Y, SUZUKI H, KUDO H, et al. Synthesis and properties of fluorine-containing poly(ether)s with pendant hydroxyl groups by the polyaddition of Bis(oxetane)s and bisphenol AF[J]. Polymer Journal, 2004, 36(2): 114-122. doi: 10.1295/polymj.36.114
[13] BARADIE B, SHOICHET M S. Novel fluoro-terpolymers for coatings applications[J]. Macromolecules, 2005, 38(13): 5560-5568. doi: 10.1021/ma047792s
[14] MATSUSHIMA A, LIU X H, OKADA H, et al. Bisphenol AF is a full agonist for the estrogen receptor ERα but a highly specific antagonist for ERβ[J]. Environmental Health Perspectives, 2010, 118(9): 1267-1272. doi: 10.1289/ehp.0901819
[15] YANG Y J, GUAN J, YIN J, et al. Urinary levels of bisphenol analogues in residents living near a manufacturing plant in South China[J]. Chemosphere, 2014, 112: 481-486. doi: 10.1016/j.chemosphere.2014.05.004
[16] JIN H B, XIE J H, MAO L L, et al. Bisphenol analogue concentrations in human breast milk and their associations with postnatal infant growth[J]. Environmental Pollution, 2020, 259: 113779. doi: 10.1016/j.envpol.2019.113779
[17] LANG I A, GALLOWAY T S, SCARLETT A, et al. Association of urinary bisphenol A concentration with medical disorders and laboratory abnormalities in adults[J]. JAMA, 2008, 300(11): 1303-1310. doi: 10.1001/jama.300.11.1303
[18] SHANKAR A, TEPPALA S. Relationship between urinary bisphenol A levels and diabetes mellitus[J]. The Journal of Clinical Endocrinology and Metabolism, 2011, 96(12): 3822-3826. doi: 10.1210/jc.2011-1682
[19] SILVER M K, O’NEILL M S, SOWERS M R, et al. Urinary bisphenol A and type-2 diabetes in U. S. adults: Data from NHANES 2003-2008[J]. PLoS One, 2011, 6(10): e26868. doi: 10.1371/journal.pone.0026868
[20] HWANG S, LIM J E, CHOI Y, et al. Bisphenol A exposure and type 2 diabetes mellitus risk: A meta-analysis[J]. BMC Endocrine Disorders, 2018, 18(1): 81. doi: 10.1186/s12902-018-0310-y
[21] SONG Y, CHOU E L, BAECKER A, et al. Endocrine-disrupting chemicals, risk of type 2 diabetes, and diabetes-related metabolic traits: A systematic review and meta-analysis[J]. Journal of Diabetes, 2016, 8(4): 516-532. doi: 10.1111/1753-0407.12325
[22] DUAN Y S, YAO Y M, WANG B, et al. Association of urinary concentrations of bisphenols with type 2 diabetes mellitus: A case-control study[J]. Environmental Pollution, 2018, 243: 1719-1726. doi: 10.1016/j.envpol.2018.09.093
[23] ANGLE B M, DO R P, PONZI D, et al. Metabolic disruption in male mice due to fetal exposure to low but not high doses of bisphenol A (BPA): Evidence for effects on body weight, food intake, adipocytes, leptin, adiponectin, insulin and glucose regulation[J]. Reproductive Toxicology, 2013, 42: 256-268. doi: 10.1016/j.reprotox.2013.07.017
[24] ALONSO-MAGDALENA P, MORIMOTO S, RIPOLL C, et al. The estrogenic effect of bisphenol A disrupts pancreatic β-cell function in vivo and induces insulin resistance[J]. Environmental Health Perspectives, 2006, 114(1): 106-112. doi: 10.1289/ehp.8451
[25] GYIMAH E, DONG X, XU H, et al. Embryonic exposure to low concentrations of bisphenol A and S altered genes related to pancreatic β-cell development and DNA methyltransferase in zebrafish[J]. Archives of Environmental Contamination and Toxicology, 2021, 80(2): 450-460. doi: 10.1007/s00244-021-00812-8
[26] NADAL A, ALONSO-MAGDALENA P, SORIANO S, et al. The pancreatic β-cell as a target of estrogens and xenoestrogens: Implications for blood glucose homeostasis and diabetes[J]. Molecular and Cellular Endocrinology, 2009, 304(1/2): 63-68.
[27] ALONSO-MAGDALENA P, VIEIRA E, SORIANO S, et al. Bisphenol A exposure during pregnancy disrupts glucose homeostasis in mothers and adult male offspring[J]. Environmental Health Perspectives, 2010, 118(9): 1243-1250. doi: 10.1289/ehp.1001993
[28] FANG F F, CHEN D L, YU P, et al. Effects of bisphenol A on glucose homeostasis and brain insulin signaling pathways in male mice[J]. General and Comparative Endocrinology, 2015, 212: 44-50. doi: 10.1016/j.ygcen.2015.01.017
[29] SORIANO S, ALONSO-MAGDALENA P, GARCÍA-ARÉVALO M, et al. Rapid insulinotropic action of low doses of bisphenol-A on mouse and human islets of Langerhans: Role of estrogen receptor Β[J]. PLoS One, 2012, 7(2): e31109. doi: 10.1371/journal.pone.0031109
[30] SONG L Q, XIA W, ZHOU Z, et al. Low-level phenolic estrogen pollutants impair islet morphology and β-cell function in isolated rat islets[J]. Journal of Endocrinology, 2012, 215(2): 303-311. doi: 10.1530/JOE-12-0219
[31] ADACHI T, YASUDA K, MORI C, et al. Promoting insulin secretion in pancreatic islets by means of bisphenol A and nonylphenol via intracellular estrogen receptors[J]. Food and Chemical Toxicology, 2005, 43(5): 713-719. doi: 10.1016/j.fct.2005.01.009
[32] BABILONI-CHUST I, dos SANTOS R S, MEDINA-GALI R M, et al. G protein-coupled estrogen receptor activation by bisphenol-a disrupts the protection from apoptosis conferred by the estrogen receptors ERα and ERβ in pancreatic beta cells[J]. Environment International, 2022, 164: 107250. doi: 10.1016/j.envint.2022.107250
[33] BORONAT-BELDA T, FERRERO H, AL-ABDULLA R, et al. Bisphenol-A exposure during pregnancy alters pancreatic β-cell division and mass in male mice offspring: A role for ERβ[J]. Food and Chemical Toxicology, 2020, 145: 111681. doi: 10.1016/j.fct.2020.111681
[34] NADAL A, ROPERO A B, LARIBI O, et al. Nongenomic actions of estrogens and xenoestrogens by binding at a plasma membrane receptor unrelated to estrogen receptor α and estrogen receptor β[J]. Proceedings of the National Academy of Sciences of the United States of America, 2000, 97(21): 11603-11608.
[35] CARCHIA E, PORRECA I, ALMEIDA P J, et al. 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[J]. Cell Death & Disease, 2015, 6(10): e1959.
[36] KITAMURA S, SUZUKI T, SANOH S, et al. Comparative study of the endocrine-disrupting activity of bisphenol A and 19 related compounds[J]. Toxicological Sciences, 2005, 84(2): 249-259. doi: 10.1093/toxsci/kfi074
[37] SONG M Y, LIANG D, LIANG Y, et al. Assessing developmental toxicity and estrogenic activity of halogenated bisphenol A on zebrafish (Danio rerio)[J]. Chemosphere, 2014, 112: 275-281. doi: 10.1016/j.chemosphere.2014.04.084
[38] PINTO-JUNIOR D C, SILVA K S, MICHALANI M L, et al. Advanced glycation end products-induced insulin resistance involves repression of skeletal muscle GLUT4 expression[J]. Scientific Reports, 2018, 8(1): 8109. doi: 10.1038/s41598-018-26482-6
[39] COUGHLAN M T, THORBURN D R, PENFOLD S A, et al. RAGE-induced cytosolic ROS promote mitochondrial superoxide generation in diabetes[J]. Journal of the American Society of Nephrology, 2009, 20(4): 742-752. doi: 10.1681/ASN.2008050514
[40] WALKE P B, BANSODE S B, MORE N P, et al. Molecular investigation of glycated insulin-induced insulin resistance via insulin signaling and AGE-RAGE axis[J]. Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, 2021, 1867(2): 166029. doi: 10.1016/j.bbadis.2020.166029
[41] YAN S F, RAMASAMY R, NAKA Y, et al. Glycation, inflammation, and RAGE: A scaffold for the macrovascular complications of diabetes and beyond[J]. Circulation Research, 2003, 93(12): 1159-1169. doi: 10.1161/01.RES.0000103862.26506.3D
[42] RAMASAMY R, YAN S F, SCHMIDT A M. Receptor for AGE (RAGE): Signaling mechanisms in the pathogenesis of diabetes and its complications[J]. Annals of the New York Academy of Sciences, 2011, 1243: 88-102. doi: 10.1111/j.1749-6632.2011.06320.x
[43] BHATTACHARYA R, ALAM M R, KAMAL M A, et al. AGE-RAGE axis culminates into multiple pathogenic processes: A central road to neurodegeneration[J]. Frontiers in Molecular Neuroscience, 2023, 16: 1155175. doi: 10.3389/fnmol.2023.1155175
[44] LEE J H, MELLADO-GIL J M, BAHN Y J, et al. Protection from β-cell apoptosis by inhibition of TGF-β/Smad3 signaling[J]. Cell Death & Disease, 2020, 11(3): 184.
[45] SHIGETO M, RAMRACHEYA R, TARASOV A I, et al. GLP-1 stimulates insulin secretion by PKC-dependent TRPM4 and TRPM5 activation[J]. The Journal of Clinical Investigation, 2015, 125(12): 4714-4728. doi: 10.1172/JCI81975
[46] ASHCROFT F M, PROKS P, SMITH P A, et al. Stimulus-secretion coupling in pancreatic β cells[J]. Journal of Cellular Biochemistry, 1994, 55(S1994A): 54-65. doi: 10.1002/jcb.240550007
[47] KAWANO S, SHOJI S, ICHINOSE S, et al. Characterization of Ca2+ signaling pathways in human mesenchymal stem cells[J]. Cell Calcium, 2002, 32(4): 165-174. doi: 10.1016/S0143416002001240
[48] KAHN S E. The relative contributions of insulin resistance and beta-cell dysfunction to the pathophysiology of Type 2 diabetes[J]. Diabetologia, 2003, 46(1): 3-19. doi: 10.1007/s00125-002-1009-0