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Open Access 01-12-2024 | Gestational Diabetes | Review

Endocrine disrupting chemicals: gestational diabetes and beyond

Authors: Tridip Mitra, Richa Gulati, Krithika Ramachandran, Rohan Rajiv, Elizabeth Ann L. Enninga, Chris K Pierret, Sajeetha Kumari R, Rajiv Janardhanan

Published in: Diabetology & Metabolic Syndrome | Issue 1/2024

Abstract

Gestational Diabetes Mellitus (GDM) has been on the rise for the last two decades along with the growing incidence of obesity. The ubiquitous use of Endocrine-Disrupting Chemicals (EDCs) worldwide has been associated with this increase in GDM incidence. Epigenetic modifications such as DNA methylation, histone acetylation, and methylation have been associated with prenatal exposure to EDCs. EDC exposure can also drive a sustained disruption of the hypothalamus-pituitary-thyroid axis and various other signaling pathways such as thyroid signaling, PPARγ signaling, PI3K-AKT signaling. This disruption leads to impaired glucose metabolism, insulin resistance as well as β-cell dysfunction, which culminate into GDM. Persistent EDC exposure in pregnant women also increases adipogenesis, which results in gestational weight gain. Importantly, pregnant mothers transfer these EDCs to the fetus via the placenta, thus leading to other pregnancy-associated complications such as intrauterine growth restriction (IUGR), and large for gestational age neonates. Furthermore, this early EDC exposure of the fetus increases the susceptibility of the infant to metabolic diseases in early life. The transgenerational impact of EDCs is also associated with higher vascular tone, cognitive aberrations, and enhanced susceptibility to lifestyle disorders including reproductive health anomalies. The review focuses on the impact of environmental toxins in inducing epigenetic alterations and increasing the susceptibility to metabolic diseases during pregnancy needs to be extensively studied such that interventions can be developed to break this vicious cycle. Furthermore, the use of EDC-associated ExomiRs from the serum of patients can help in the early diagnosis of GDM, thereby leading to triaging of patients based on increasing risk factor of the clinicopathological condition.

Sacks DA, Hadden DR, Maresh M, et al. Frequency of gestational diabetes mellitus at collaborating centers based on IADPSG consensus panel-recommended criteria: the hyperglycemia and adverse pregnancy outcome (HAPO) study. Diabetes Care. 2012;35(3):526–8. https://doi.org/10.2337/dc11-1641.CrossRefPubMedPubMedCentral

Wang H, Li N, Chivese T, et al. IDF Diabetes Atlas: estimation of Global and Regional Gestational Diabetes Mellitus Prevalence for 2021 by International Association of Diabetes in Pregnancy Study Group’s Criteria. Diabetes Res Clin Pract. 2022;183:109050. https://doi.org/10.1016/j.diabres.2021.109050.CrossRefPubMed

Farahvar S, Walfisch A, Sheiner E. Gestational diabetes risk factors and long-term consequences for both mother and offspring: a literature review. Expert Rev Endocrinol Metab. 2019;14(1):63–74. https://doi.org/10.1080/17446651.2018.1476135.CrossRefPubMed

Hasbullah FY, Mohd Yusof BN, Shariff ZM, Rejali Z, Yong HY, Mitri J. Factors associated with dietary glycemic index and glycemic load in pregnant women and risk for gestational diabetes mellitus. Int J Food Sci Nutr. 2020;71(4):516–24. https://doi.org/10.1080/09637486.2019.1686752.CrossRefPubMed

Bellavia A, Mínguez-Alarcón L, Ford JB, et al. Association of self-reported personal care product use with blood glucose levels measured during pregnancy among women from a fertility clinic. Sci Total Environ. 2019;695:133855. https://doi.org/10.1016/j.scitotenv.2019.133855.CrossRefPubMedPubMedCentral

Kassotis CD, Vandenberg LN, Demeneix BA, Porta M, Slama R, Trasande L. Endocrine-disrupting chemicals: economic, regulatory, and policy implications. Lancet Diabetes Endocrinol. 2020;8(8):719–30. https://doi.org/10.1016/S2213-8587(20)30128-5.CrossRefPubMedPubMedCentral

Kahn LG, Philippat C, Nakayama SF, Slama R, Trasande L. Endocrine-disrupting chemicals: implications for human health. Lancet Diabetes Endocrinol. 2020;8(8):703–18. https://doi.org/10.1016/S2213-8587(20)30129-7.CrossRefPubMedPubMedCentral

Gingrich J, Ticiani E, Veiga-Lopez A. Placenta disrupted: endocrine disrupting chemicals and pregnancy. Trends Endocrinol Metab. 2020;31(7):508–24. https://doi.org/10.1016/j.tem.2020.03.003.CrossRefPubMedPubMedCentral

Braun JM. Early-life exposure to EDCs: role in childhood obesity and neurodevelopment. Nat Rev Endocrinol. 2017;13(3):161–73. https://doi.org/10.1038/nrendo.2016.186.CrossRefPubMed

10.

Miller RG, Costacou T, Orchard TJ. Risk factor modeling for Cardiovascular Disease in Type 1 diabetes in the Pittsburgh Epidemiology of Diabetes Complications (EDC) study: a comparison with the Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and complications Study (DCCT/EDIC). Diabetes. 2019;68(2):409–19. https://doi.org/10.2337/db18-0515.CrossRefPubMed

11.

Chen Y, Xiao H, Namat A, et al. Association between trimester-specific exposure to thirteen endocrine disrupting chemicals and preterm birth: comparison of three statistical models. Sci Total Environ. 2022;851(Pt 2):158236. https://doi.org/10.1016/j.scitotenv.2022.158236.CrossRefPubMed

12.

Kunysz M, Mora-Janiszewska O, Darmochwał-Kolarz D. Epigenetic Modifications Associated with exposure to endocrine disrupting chemicals in patients with gestational diabetes Mellitus. Int J Mol Sci. 2021;22(9). https://doi.org/10.3390/ijms22094693.

13.

Birru RL, Liang HW, Farooq F, et al. A pathway level analysis of PFAS exposure and risk of gestational diabetes mellitus. Environ Health. 2021;20(1):63. https://doi.org/10.1186/s12940-021-00740-z.CrossRefPubMedPubMedCentral

14.

Gulati R, Nandi D, Sarkar K, et al. Exosomes as theranostic targets: implications for the clinical prognosis of aggressive cancers. Front Mol Biosci. 2022;9:890768. https://doi.org/10.3389/fmolb.2022.890768.CrossRefPubMedPubMedCentral

15.

Mitra T, Gulati R, Uppal A, et al. Prospecting of exosomal-miRNA signatures as prognostic marker for gestational diabetes mellitus and other adverse pregnancy outcomes. Front Endocrinol (Lausanne). 2023;14:1097337. https://doi.org/10.3389/fendo.2023.1097337.CrossRefPubMed

16.

Martin L, Zhang Y, First O, et al. Lifestyle interventions to reduce endocrine-disrupting phthalate and phenol exposures among reproductive age men and women: a review and future steps. Environ Int. 2022;170:107576. https://doi.org/10.1016/j.envint.2022.107576.CrossRefPubMedPubMedCentral

17.

Menale C, Mita DG, Diano N, Diano S. Adverse effects of Bisphenol A exposure on glucose metabolism regulation. Open Biotechnol J. 2016;10(1):122–30. https://doi.org/10.2174/1874070701610010122.CrossRef

18.

Stahlhut RW, Myers JP, Taylor JA, Nadal A, Dyer JA, Vom Saal FS. Experimental BPA exposure and glucose-stimulated insulin response in adult men and women. J Endocr Soc. 2018;2(10):1173–87. https://doi.org/10.1210/js.2018-00151.CrossRefPubMedPubMedCentral

19.

Rochester JR. Bisphenol A and human health: a review of the literature. Reprod Toxicol. 2013;42:132–55. https://doi.org/10.1016/j.reprotox.2013.08.008.CrossRefPubMed

20.

Braun JM, Muckle G, Arbuckle T, et al. Associations of prenatal urinary bisphenol A concentrations with child behaviors and cognitive abilities. Environ Health Perspect. 2017;125(6):067008. https://doi.org/10.1289/EHP984.CrossRefPubMedPubMedCentral

21.

Zhang W, Xia W, Liu W, et al. Exposure to Bisphenol a substitutes and Gestational Diabetes Mellitus: a prospective cohort study in China. Front Endocrinol (Lausanne). 2019;10:262. https://doi.org/10.3389/fendo.2019.00262.CrossRefPubMed

22.

Eberle C, Stichling S. Environmental health influences in pregnancy and risk of gestational diabetes mellitus: a systematic review. BMC Public Health. 2022;22(1):1572. https://doi.org/10.1186/s12889-022-13965-5.CrossRefPubMedPubMedCentral

23.

Chiu YH, Mínguez-Alarcón L, Ford JB, et al. Trimester-specific urinary bisphenol A concentrations and blood glucose levels among pregnant women from a fertility clinic. J Clin Endocrinol Metab. 2017;102(4):1350–7. https://doi.org/10.1210/jc.2017-00022.CrossRefPubMedPubMedCentral

24.

Bellavia A, Cantonwine DE, Meeker JD, et al. Pregnancy urinary bisphenol-A concentrations and glucose levels across BMI categories. Environ Int. 2018;113:35–41. https://doi.org/10.1016/j.envint.2018.01.012.CrossRefPubMedPubMedCentral

25.

Alonso-Magdalena P, Quesada I, Nadal Á. Prenatal exposure to BPA and offspring outcomes: the Diabesogenic Behavior of BPA. Dose Response. 2015;13(2):1559325815590395. https://doi.org/10.1177/1559325815590395.CrossRefPubMedPubMedCentral

26.

Jacovetti C, Abderrahmani A, Parnaud G, et al. MicroRNAs contribute to compensatory β cell expansion during pregnancy and obesity. J Clin Invest. 2012;122(10):3541–51. https://doi.org/10.1172/JCI64151.CrossRefPubMedPubMedCentral

27.

Wei J, Ding D, Wang T, Liu Q, Lin Y. MiR-338 controls BPA-triggered pancreatic islet insulin secretory dysfunction from compensation to decompensation by targeting Pdx-1. FASEB J. 2017;31(12):5184–95. https://doi.org/10.1096/fj.201700282R.CrossRefPubMed

28.

Phrakonkham P, Viengchareun S, Belloir C, Lombès M, Artur Y, Canivenc-Lavier MC. Dietary xenoestrogens differentially impair 3T3-L1 preadipocyte differentiation and persistently affect leptin synthesis. J Steroid Biochem Mol Biol. 2008;110(1–2):95–103. https://doi.org/10.1016/j.jsbmb.2008.02.006.CrossRefPubMed

29.

Masuno H, Iwanami J, Kidani T, Sakayama K, Honda K. Bisphenol a accelerates terminal differentiation of 3T3-L1 cells into adipocytes through the phosphatidylinositol 3-kinase pathway. Toxicol Sci. 2005;84(2):319–27. https://doi.org/10.1093/toxsci/kfi088.CrossRefPubMed

30.

Ariemma F, D’Esposito V, Liguoro D, et al. Low-dose Bisphenol-A impairs adipogenesis and generates dysfunctional 3T3-L1 adipocytes. PLoS ONE. 2016;11(3):e0150762. https://doi.org/10.1371/journal.pone.0150762.CrossRefPubMedPubMedCentral

31.

Ohlstein JF, Strong AL, McLachlan JA, Gimble JM, Burow ME, Bunnell BA. Bisphenol a enhances adipogenic differentiation of human adipose stromal/stem cells. J Mol Endocrinol. 2014;53(3):345–53. https://doi.org/10.1530/JME-14-0052.CrossRefPubMedPubMedCentral

32.

Angle BM, Do RP, 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. Reprod Toxicol. 2013;42:256–68. https://doi.org/10.1016/j.reprotox.2013.07.017.CrossRefPubMed

33.

Carwile JL, Michels KB. Urinary bisphenol A and obesity: NHANES 2003–2006. Environ Res. 2011;111(6):825–30. https://doi.org/10.1016/j.envres.2011.05.014.CrossRefPubMedPubMedCentral

34.

Liao SL, Tsai MH, Lai SH, et al. Prenatal exposure to bisphenol-A is associated with toll-like receptor-induced cytokine suppression in neonates. Pediatr Res. 2016;79(3):438–44. https://doi.org/10.1038/pr.2015.234.CrossRefPubMed

35.

Stanirowski PJ, Szukiewicz D, Pyzlak M, Abdalla N, Sawicki W, Cendrowski K. Analysis of correlations between the placental expression of glucose transporters glut-1, GLUT-4 and Glut-9 and selected maternal and fetal parameters in pregnancies complicated by diabetes mellitus. J Maternal-Fetal Neonatal Med. 2017;32(4):650–9. https://doi.org/10.1080/14767058.2017.1387897.CrossRef

36.

Binder AM, Corvalan C, Pereira A, et al. Prepubertal and Pubertal Endocrine-Disrupting Chemical exposure and breast density among Chilean adolescents. Cancer Epidemiol Biomarkers Prev. 2018;27(12):1491–9. https://doi.org/10.1158/1055-9965.EPI-17-0813.CrossRefPubMedPubMedCentral

37.

Lokate M, Peeters PH, Peelen LM, Haars G, Veldhuis WB, van Gils CH. Mammographic density and breast cancer risk: the role of the fat surrounding the fibroglandular tissue. Breast Cancer Res. 2011;13(5):R103. https://doi.org/10.1186/bcr3044.CrossRefPubMedPubMedCentral

38.

Vrachnis N, Loukas N, Vrachnis D, et al. A systematic review of Bisphenol A from Dietary and Non-dietary sources during pregnancy and its possible connection with fetal growth restriction: investigating its potential effects and the window of fetal vulnerability. Nutrients. 2021;13(7). https://doi.org/10.3390/nu13072426.

39.

De Felice B, Manfellotto F, Palumbo A, et al. Genome-wide microRNA expression profiling in placentas from pregnant women exposed to BPA. BMC Med Genomics. 2015;8:56. https://doi.org/10.1186/s12920-015-0131-z.CrossRefPubMedPubMedCentral

40.

Martínez-Ibarra A, Martínez-Razo LD, Vázquez-Martínez ER, et al. Unhealthy levels of phthalates and bisphenol A in Mexican pregnant women with gestational diabetes and its association to altered expression of miRNAs involved with metabolic disease. Int J Mol Sci. 2019;20(13). https://doi.org/10.3390/ijms20133343.

41.

Zhao C, Dong J, Jiang T, et al. Early second-trimester serum miRNA profiling predicts gestational diabetes mellitus. PLoS ONE. 2011;6(8):e23925. https://doi.org/10.1371/journal.pone.0023925.CrossRefPubMedPubMedCentral

42.

Mao Z, Xia W, Huo W, et al. Pancreatic impairment and Igf2 hypermethylation induced by developmental exposure to bisphenol A can be counteracted by maternal folate supplementation. J Appl Toxicol. 2017;37(7):825–35. https://doi.org/10.1002/jat.3430.CrossRefPubMed

43.

Chang H, Wang D, Xia W, et al. Epigenetic disruption and glucose homeostasis changes following low-dose maternal bisphenol A exposure. Toxicol Res (Camb). 2016;5(5):1400–9. https://doi.org/10.1039/c6tx00047a.CrossRefPubMed

44.

Grzęda E, Matuszewska J, Ziarniak K, et al. Animal Foetal Models of Obesity and Diabetes - from Laboratory to clinical settings. Front Endocrinol (Lausanne). 2022;13:785674. https://doi.org/10.3389/fendo.2022.785674.CrossRefPubMed

45.

Koch HM, Lorber M, Christensen KLY, Pälmke C, Koslitz S, Brüning T. Identifying sources of phthalate exposure with human biomonitoring: results of a 48 h fasting study with urine collection and personal activity patterns. Int J Hyg Environ Health. 2013;216(6):672–81. https://doi.org/10.1016/j.ijheh.2012.12.002.CrossRefPubMed

46.

James-Todd TM, Meeker JD, Huang T, et al. Pregnancy urinary phthalate metabolite concentrations and gestational diabetes risk factors. Environ Int. 2016;96:118–26. https://doi.org/10.1016/j.envint.2016.09.009.CrossRefPubMedPubMedCentral

47.

Rodríguez-Carmona Y, Cantoral A, Trejo-Valdivia B, et al. Phthalate exposure during pregnancy and long-term weight gain in women. Environ Res. 2019;169:26–32. https://doi.org/10.1016/j.envres.2018.10.014.CrossRefPubMed

48.

Feige JN, Gelman L, Rossi D, et al. The endocrine disruptor monoethyl-hexyl-phthalate is a selective peroxisome proliferator-activated receptor gamma modulator that promotes adipogenesis. J Biol Chem. 2007;282(26):19152–66. https://doi.org/10.1074/jbc.M702724200.CrossRefPubMed

49.

Watt J, Schlezinger JJ. Structurally-diverse, PPARγ-activating environmental toxicants induce adipogenesis and suppress osteogenesis in bone marrow mesenchymal stromal cells. Toxicology. 2015;331:66–77. https://doi.org/10.1016/j.tox.2015.03.006.CrossRefPubMed

50.

Rajesh P, Balasubramanian K. Phthalate exposure in utero causes epigenetic changes and impairs insulin signalling. J Endocrinol. 2014;223(1):47–66. https://doi.org/10.1530/JOE-14-0111.CrossRefPubMed

51.

Chen M, Zhao S, Guo WH, et al. Maternal exposure to Di-n-butyl phthalate (DBP) aggravate gestational diabetes mellitus via FoxM1 suppression by pSTAT1 signalling. Ecotoxicol Environ Saf. 2020;205:111154. https://doi.org/10.1016/j.ecoenv.2020.111154.CrossRefPubMed

52.

Deng T, Zhang Y, Wu Y, et al. Dibutyl phthalate exposure aggravates type 2 diabetes by disrupting the insulin-mediated PI3K/AKT signaling pathway. Toxicol Lett. 2018;290:1–9. https://doi.org/10.1016/j.toxlet.2018.03.004.CrossRefPubMed

53.

Werner EF, Braun JM, Yolton K, Khoury JC, Lanphear BP. The association between maternal urinary phthalate concentrations and blood pressure in pregnancy: the HOME Study. Environ Health. 2015;14:75. https://doi.org/10.1186/s12940-015-0062-3.CrossRefPubMedPubMedCentral

54.

Zhu Y, Tian F, Li H, Zhou Y, Lu J, Ge Q. Profiling maternal plasma microRNA expression in early pregnancy to predict gestational diabetes mellitus. Int J Gynaecol Obstet. 2015;130(1):49–53. https://doi.org/10.1016/j.ijgo.2015.01.010.CrossRefPubMed

55.

Addo KA, Palakodety N, Hartwell HJ, Tingare A, Fry RC. Placental microRNAs: responders to environmental chemicals and mediators of pathophysiology of the human placenta. Toxicol Rep. 2020;7:1046–56. https://doi.org/10.1016/j.toxrep.2020.08.002.CrossRefPubMedPubMedCentral

56.

Manikkam M, Tracey R, Guerrero-Bosagna C, Skinner MK. Plastics derived endocrine disruptors (BPA, DEHP and DBP) induce epigenetic transgenerational inheritance of obesity, reproductive disease and sperm epimutations. PLoS ONE. 2013;8(1):e55387. https://doi.org/10.1371/journal.pone.0055387.CrossRefPubMedPubMedCentral

57.

Stel J, Legler J. The role of epigenetics in the Latent effects of early life exposure to obesogenic endocrine disrupting chemicals. Endocrinology. 2015;156(10):3466–72. https://doi.org/10.1210/en.2015-1434.CrossRefPubMedPubMedCentral

58.

Alejandro EU, Mamerto TP, Chung G, et al. Gestational diabetes Mellitus: a harbinger of the vicious cycle of diabetes. Int J Mol Sci. 2020;21(14). https://doi.org/10.3390/ijms21145003.

59.

Sunderland EM, Hu XC, Dassuncao C, Tokranov AK, Wagner CC, Allen JG. A review of the pathways of human exposure to poly- and perfluoroalkyl substances (PFASs) and present understanding of health effects. J Expo Sci Environ Epidemiol. 2019;29(2):131–47. https://doi.org/10.1038/s41370-018-0094-1.CrossRefPubMed

60.

Pinas V, Van Dijk C, Weber R. Inventory and action plan for PFOS and related substances in Suriname as basis for Stockholm Convention implementation. Emerg Contam. 2020;6:421–31. https://doi.org/10.1016/j.emcon.2020.10.002.CrossRef

61.

Yan S, Zhang H, Zheng F, Sheng N, Guo X, Dai J. Perfluorooctanoic acid exposure for 28 days affects glucose homeostasis and induces insulin hypersensitivity in mice. Sci Rep. 2015;5:11029. https://doi.org/10.1038/srep11029.CrossRefPubMedPubMedCentral

62.

Fang X, Gao G, Xue H, Zhang X, Wang H. Exposure of perfluorononanoic acid suppresses the hepatic insulin signal pathway and increases serum glucose in rats. Toxicology. 2012;294(2–3):109–15. https://doi.org/10.1016/j.tox.2012.02.008.CrossRefPubMed

63.

Hines EP, White SS, Stanko JP, Gibbs-Flournoy EA, Lau C, Fenton SE. Phenotypic dichotomy following developmental exposure to perfluorooctanoic acid (PFOA) in female CD-1 mice: low doses induce elevated serum leptin and insulin, and overweight in mid-life. Mol Cell Endocrinol. 2009;304(1–2):97–105. https://doi.org/10.1016/j.mce.2009.02.021.CrossRefPubMed

64.

Rahman ML, Zhang C, Smarr MM, et al. Persistent organic pollutants and gestational diabetes: a multi-center prospective cohort study of healthy US women. Environ Int. 2019;124:249–58. https://doi.org/10.1016/j.envint.2019.01.027.CrossRefPubMed

65.

Matilla-Santander N, Valvi D, Lopez-Espinosa MJ, et al. Exposure to Perfluoroalkyl substances and metabolic outcomes in pregnant women: evidence from the Spanish INMA birth cohorts. Environ Health Perspect. 2017;125(11):117004. https://doi.org/10.1289/EHP1062.CrossRefPubMedPubMedCentral

66.

Jensen RC, Glintborg D, Timmermann CAG, et al. Perfluoroalkyl substances and glycemic status in pregnant Danish women: the Odense Child Cohort. Environ Int. 2018;116:101–7. https://doi.org/10.1016/j.envint.2018.04.010.CrossRefPubMed

67.

Marks KJ, Jeddy Z, Flanders WD, et al. Maternal serum concentrations of perfluoroalkyl substances during pregnancy and gestational weight gain: the Avon Longitudinal Study of parents and children. Reprod Toxicol. 2019;90:8–14. https://doi.org/10.1016/j.reprotox.2019.08.003.CrossRefPubMedPubMedCentral

68.

Mitro SD, Sagiv SK, Rifas-Shiman SL, et al. Per- and polyfluoroalkyl substance exposure, Gestational Weight Gain, and Postpartum Weight changes in Project viva. Obes (Silver Spring). 2020;28(10):1984–92. https://doi.org/10.1002/oby.22933.CrossRef

69.

Li CH, Ren XM, Cao LY, Qin WP, Guo LH. Investigation of binding and activity of perfluoroalkyl substances to the human peroxisome proliferator-activated receptor β/δ. Environ Sci Process Impacts. 2019;21(11):1908–14. https://doi.org/10.1039/c9em00218a.CrossRefPubMed

70.

Liu H, Hu W, Li X, et al. Do perfluoroalkyl substances aggravate the occurrence of obesity-associated glucolipid metabolic disease? Environ Res. 2021;202:111724. https://doi.org/10.1016/j.envres.2021.111724.CrossRefPubMed

71.

Blake BE, Cope HA, Hall SM, et al. Evaluation of maternal, embryo, and placental effects in CD-1 mice following gestational exposure to Perfluorooctanoic Acid (PFOA) or hexafluoropropylene oxide dimer acid (HFPO-DA or GenX). Environ Health Perspect. 2020;128(2):27006. https://doi.org/10.1289/EHP6233.CrossRefPubMed

72.

Parsons J, Sparrow K, Ismail K, Hunt K, Rogers H, Forbes A. Experiences of gestational diabetes and gestational diabetes care: a focus group and interview study. BMC Pregnancy Childbirth. 2018;18(1):25. https://doi.org/10.1186/s12884-018-1657-9.CrossRefPubMedPubMedCentral

73.

Berg V, Nøst TH, Hansen S, et al. Assessing the relationship between perfluoroalkyl substances, thyroid hormones and binding proteins in pregnant women; a longitudinal mixed effects approach. Environ Int. 2015;77:63–9. https://doi.org/10.1016/j.envint.2015.01.007.CrossRefPubMed

74.

Berg V, Nøst TH, Pettersen RD, et al. Persistent Organic pollutants and the Association with maternal and infant thyroid homeostasis: a Multipollutant Assessment. Environ Health Perspect. 2017;125(1):127–33. https://doi.org/10.1289/EHP152.CrossRefPubMed

75.

Ballesteros V, Costa O, Iñiguez C, Fletcher T, Ballester F, Lopez-Espinosa MJ. Exposure to perfluoroalkyl substances and thyroid function in pregnant women and children: a systematic review of epidemiologic studies. Environ Int. 2017;99:15–28. https://doi.org/10.1016/j.envint.2016.10.015.CrossRefPubMed

76.

Manzano-Salgado CB, Casas M, Lopez-Espinosa MJ, et al. Transfer of perfluoroalkyl substances from mother to fetus in a Spanish birth cohort. Environ Res. 2015;142:471–8. https://doi.org/10.1016/j.envres.2015.07.020.CrossRefPubMed

77.

Mogensen UB, Grandjean P, Nielsen F, Weihe P, Budtz-Jørgensen E. Breastfeeding as an exposure pathway for Perfluorinated Alkylates. Environ Sci Technol. 2015;49(17):10466–73. https://doi.org/10.1021/acs.est.5b02237.CrossRefPubMedPubMedCentral

78.

Kupsco A, Lee JJ, Prada D, et al. Marine pollutant exposures and human milk extracellular vesicle-microRNAs in a mother-infant cohort from the Faroe Islands. Environ Int. 2022;158:106986. https://doi.org/10.1016/j.envint.2021.106986.CrossRefPubMed

79.

Guerrero-Preston R, Goldman LR, Brebi-Mieville P, et al. Global DNA hypomethylation is associated with in utero exposure to cotinine and perfluorinated alkyl compounds. Epigenetics. 2010;5(6):539–46. https://doi.org/10.4161/epi.5.6.12378.CrossRefPubMedPubMedCentral

80.

Kobayashi S, Azumi K, Goudarzi H, et al. Effects of prenatal perfluoroalkyl acid exposure on cord blood IGF2/H19 methylation and ponderal index: the Hokkaido Study. J Expo Sci Environ Epidemiol. 2017;27(3):251–9. https://doi.org/10.1038/jes.2016.50.CrossRefPubMed

81.

Ku MS, Pan WC, Huang YT, et al. Associations between prenatal exposure to perfluoroalkyl substances, hypomethylation of MEST imprinted gene and birth outcomes. Environ Pollut. 2022;304:119183. https://doi.org/10.1016/j.envpol.2022.119183.CrossRefPubMed

82.

Blake BE, Fenton SE. Early life exposure to per- and polyfluoroalkyl substances (PFAS) and latent health outcomes: a review including the placenta as a target tissue and possible driver of peri- and postnatal effects. Toxicology. 2020;443:152565. https://doi.org/10.1016/j.tox.2020.152565.CrossRefPubMed

83.

Bergman Å, Heindel JJ, Jobling S, Kidd KA, Thomas Zoeller R. State of the Science of Endocrine Disrupting Chemicals-2012 INTER-ORGANIZATION PROGRAMME FOR THE SOUND MANAGEMENT OF CHEMICALS.

84.

Li XT, Yu PF, Gao Y, et al. Association between Plasma Metal Levels and diabetes risk: a case-control study in China. Biomed Environ Sci. 2017;30(7):482–91. https://doi.org/10.3967/bes2017.064.CrossRefPubMed

85.

Wang X, Mukherjee B, Park SK. Associations of cumulative exposure to heavy metal mixtures with obesity and its comorbidities among U.S. adults in NHANES 2003–2014. Environ Int. 2018;121(Pt 1):683–94. https://doi.org/10.1016/j.envint.2018.09.035.CrossRefPubMedPubMedCentral

86.

Padilla MA, Elobeid M, Ruden DM, Allison DB. An examination of the association of selected toxic metals with total and central obesity indices: NHANES 99– 02. Int J Environ Res Public Health. 2010;7(9):3332–47. https://doi.org/10.3390/ijerph7093332.CrossRefPubMedPubMedCentral

87.

Romano ME, Enquobahrie DA, Simpson CD, Checkoway H, Williams MA. A case-cohort study of Cadmium Body Burden and Gestational Diabetes Mellitus in American Women. Environ Health Perspect. 2015;123(10):993–8. https://doi.org/10.1289/ehp.1408282.CrossRefPubMedPubMedCentral

88.

Tinkov AA, Filippini T, Ajsuvakova OP, et al. The role of cadmium in obesity and diabetes. Sci Total Environ. 2017;601–602:741–55. https://doi.org/10.1016/j.scitotenv.2017.05.224.CrossRefPubMed

89.

Kawakami T, Nishiyama K, Kadota Y, Sato M, Inoue M, Suzuki S. Cadmium modulates adipocyte functions in metallothionein-null mice. Toxicol Appl Pharmacol. 2013;272(3):625–36. https://doi.org/10.1016/j.taap.2013.07.015.CrossRefPubMed

90.

Lee EJ, Moon JY, Yoo BS. Cadmium inhibits the differentiation of 3T3-L1 preadipocyte through the C/EBPα and PPARγ pathways. Drug Chem Toxicol. 2012;35(2):225–31. https://doi.org/10.3109/01480545.2011.591401.CrossRefPubMed

91.

Salmeri N, Villanacci R, Ottolina J, et al. Maternal Arsenic exposure and gestational diabetes: a systematic review and Meta-analysis. Nutrients. 2020;12(10). https://doi.org/10.3390/nu12103094.

92.

Yang B, Fu J, Zheng H, et al. Deficiency in the nuclear factor E2-related factor 2 renders pancreatic β-cells vulnerable to arsenic-induced cell damage. Toxicol Appl Pharmacol. 2012;264(3):315–23. https://doi.org/10.1016/j.taap.2012.09.012.CrossRefPubMedPubMedCentral

93.

Li W, Wu L, Sun Q, et al. MicroRNA-191 blocking the translocation of GLUT4 is involved in arsenite-induced hepatic insulin resistance through inhibiting the IRS1/AKT pathway. Ecotoxicol Environ Saf. 2021;215:112130. https://doi.org/10.1016/j.ecoenv.2021.112130.CrossRefPubMed

94.

Soomro MH, Baiz N, Huel G, et al. Exposure to heavy metals during pregnancy related to gestational diabetes mellitus in diabetes-free mothers. Sci Total Environ. 2019;656:870–6. https://doi.org/10.1016/j.scitotenv.2018.11.422.CrossRefPubMed

95.

Peng S, Liu L, Zhang X, et al. A nested case-control study indicating heavy metal residues in meconium associate with maternal gestational diabetes mellitus risk. Environ Health. 2015;14:19. https://doi.org/10.1186/s12940-015-0004-0.CrossRefPubMedPubMedCentral

96.

Onat T, Demir Caltekin M, Turksoy VA, et al. The relationship between heavy metal exposure, Trace element level, and Monocyte to HDL cholesterol ratio with gestational diabetes Mellitus. Biol Trace Elem Res. 2021;199(4):1306–15. https://doi.org/10.1007/s12011-020-02499-9.CrossRefPubMed

97.

Broberg K, Ahmed S, Engström K, et al. Arsenic exposure in early pregnancy alters genome-wide DNA methylation in cord blood, particularly in boys. J Dev Orig Health Dis. 2014;5(4):288–98. https://doi.org/10.1017/S2040174414000221.CrossRefPubMedPubMedCentral

98.

Vidal AC, Semenova V, Darrah T, et al. Maternal cadmium, iron and zinc levels, DNA methylation and birth weight. BMC Pharmacol Toxicol. 2015;16:20. https://doi.org/10.1186/s40360-015-0020-2.CrossRefPubMedPubMedCentral

99.

Pilsner JR, Hu H, Ettinger A, et al. Influence of prenatal lead exposure on genomic methylation of cord blood DNA. Environ Health Perspect. 2009;117(9):1466–71. https://doi.org/10.1289/ehp.0800497.CrossRefPubMedPubMedCentral

100.

Masoud AM, Bihaqi SW, Machan JT, Zawia NH, Renehan WE. Early-life exposure to lead (pb) alters the expression of microRNA that Target Proteins Associated with Alzheimer’s Disease. J Alzheimers Dis. 2016;51(4):1257–64. https://doi.org/10.3233/JAD-151018.CrossRefPubMed

101.

Li S, Chen M, Li Y, Tollefsbol TO. Prenatal epigenetics diets play protective roles against environmental pollution. Clin Epigenetics. 2019;11(1):82. https://doi.org/10.1186/s13148-019-0659-4.CrossRefPubMedPubMedCentral

102.

Leśków A, Nawrocka M, Łątkowska M, et al. Can contamination of the environment by dioxins cause craniofacial defects? Hum Exp Toxicol. 2019;38(9):1014–23. https://doi.org/10.1177/0960327119855121.CrossRefPubMed

103.

Woeller CF, Thatcher TH, Thakar J, et al. Exposure to Heptachlorodibenzo-p-dioxin (HpCDD) regulates microRNA expression in human lung fibroblasts. J Occup Environ Med. 2019;61(Suppl 12):S82–9. https://doi.org/10.1097/JOM.0000000000001691.CrossRefPubMedPubMedCentral

104.

Marinković N, Pašalić D, Ferenčak G, Gršković B, Stavljenić Rukavina A. Dioxins and human toxicity. Arh Hig Rada Toksikol. 2010;61(4):445–53. https://doi.org/10.2478/10004-1254-61-2010-2024.CrossRefPubMed

105.

Vafeiadi M, Roumeliotaki T, Chalkiadaki G, et al. Persistent organic pollutants in early pregnancy and risk of gestational diabetes mellitus. Environ Int. 2017;98:89–95. https://doi.org/10.1016/j.envint.2016.10.005.CrossRefPubMed

106.

Thackaberry EA, Bedrick EJ, Goens MB, et al. Insulin regulation in AhR-null mice: embryonic cardiac enlargement, neonatal macrosomia, and altered insulin regulation and response in pregnant and aging AhR-null females. Toxicol Sci. 2003;76(2):407–17. https://doi.org/10.1093/toxsci/kfg229.CrossRefPubMed

107.

Merrill AK, Anderson T, Conrad K, et al. Protracted Impairment of Maternal Metabolic Health in mouse dams following pregnancy exposure to a mixture of Low Dose Endocrine-Disrupting Chemicals, a pilot study. Toxics. 2021;9(12). https://doi.org/10.3390/toxics9120346.

108.

Guida M, Marra ML, Zullo F, et al. Association between exposure to dioxin-like polychlorinated biphenyls and miR-191 expression in human peripheral blood mononuclear cells. Mutat Res. 2013;753(1):36–41. https://doi.org/10.1016/j.mrgentox.2012.12.018.CrossRefPubMed

109.

Trajkovski M, Hausser J, Soutschek J, et al. MicroRNAs 103 and 107 regulate insulin sensitivity. Nature. 2011;474(7353):649–53. https://doi.org/10.1038/nature10112.CrossRefPubMed

110.

Wang C, Yuan XG, Liu CP, Zhai SN, Zhang DW, Fu YX. Preliminary research on DNA methylation changes during murine palatogenesis induced by TCDD. J Craniomaxillofac Surg. 2017;45(5):678–84. https://doi.org/10.1016/j.jcms.2017.02.004.CrossRefPubMed

111.

Yuan X, Qiu L, Pu Y, et al. Histone acetylation is involved in TCDDinduced cleft palate formation in fetal mice. Mol Med Rep. 2016;14(2):1139–45. https://doi.org/10.3892/mmr.2016.5348.CrossRefPubMedPubMedCentral

112.

Viluksela M, Pohjanvirta R. Multigenerational and transgenerational effects of Dioxins. Int J Mol Sci. 2019;20(12). https://doi.org/10.3390/ijms20122947.

113.

Petric Z, Ružić J, Žuntar I. The controversies of parabens - an overview nowadays. Acta Pharm. 2021;71(1):17–32. https://doi.org/10.2478/acph-2021-0001.CrossRefPubMed

114.

Li Y, Xu S, Li Y, et al. Association between urinary parabens and gestational diabetes mellitus across prepregnancy body mass index categories. Environ Res. 2019;170:151–9. https://doi.org/10.1016/j.envres.2018.12.028.CrossRefPubMed

115.

Liu W, Zhou Y, Li J, et al. Parabens exposure in early pregnancy and gestational diabetes mellitus. Environ Int. 2019;126:468–75. https://doi.org/10.1016/j.envint.2019.02.040.CrossRefPubMed

116.

Bellavia A, Chiu YH, Brown FM, et al. Urinary concentrations of parabens mixture and pregnancy glucose levels among women from a fertility clinic. Environ Res. 2019;168:389–96. https://doi.org/10.1016/j.envres.2018.10.009.CrossRefPubMed

117.

Choi SI, Kwon HY, Han X, et al. Environmental obesogens (bisphenols, phthalates and parabens) and their impacts on adipogenic transcription factors in the absence of dexamethasone in 3T3-L1 cells. J Steroid Biochem Mol Biol. 2021;214:105994. https://doi.org/10.1016/j.jsbmb.2021.105994.CrossRefPubMed

118.

Elmore SE, Cano-Sancho G, La Merrill MA. Disruption of normal adipocyte development and function by methyl- and propyl- paraben exposure. Toxicol Lett. 2020;334:27–35. https://doi.org/10.1016/j.toxlet.2020.09.009.CrossRefPubMed

119.

Decker AH, Levels T. Associations between Butylparaben and thyroid levels in females aged 12 and over (NHANES, 2007–2008). Published online 2007. https://doi.org/10.57709/6464093.

120.

LaRocca J, Binder AM, McElrath TF, Michels KB. First-Trimester urine concentrations of Phthalate metabolites and phenols and Placenta miRNA expression in a cohort of U.S. women. Environ Health Perspect. 2016;124(3):380–7. https://doi.org/10.1289/ehp.1408409.CrossRefPubMed

121.

Houshmand-Oeregaard A, Schrölkamp M, Kelstrup L, et al. Increased expression of microRNA-15a and microRNA-15b in skeletal muscle from adult offspring of women with diabetes in pregnancy. Hum Mol Genet. 2018;27(10):1763–71. https://doi.org/10.1093/hmg/ddy085.CrossRefPubMed

122.

Qi S, Wang X. Decreased expression of miR-185 in serum and placenta of patients with gestational diabetes Mellitus. Clin Lab. 2019;65(12). https://doi.org/10.7754/Clin.Lab.2019.190445.

123.

Wang XC, Zhan XR, Li XY, Yu JJ, Liu XM. MicroRNA-185 regulates expression of lipid metabolism genes and improves insulin sensitivity in mice with non-alcoholic fatty liver disease. World J Gastroenterol. 2014;20(47):17914–23. https://doi.org/10.3748/wjg.v20.i47.17914.CrossRefPubMedPubMedCentral

124.

LaRocca J, Binder AM, McElrath TF, Michels KB. The impact of first trimester phthalate and phenol exposure on IGF2/H19 genomic imprinting and birth outcomes. Environ Res. 2014;133:396–406. https://doi.org/10.1016/j.envres.2014.04.032.CrossRefPubMedPubMedCentral

125.

Park CJ, Nah WH, Lee JE, Oh YS, Gye MC. Butyl paraben-induced changes in DNA methylation in rat epididymal spermatozoa. Andrologia. 2012;44(Suppl 1):187–93. https://doi.org/10.1111/j.1439-0272.2011.01162.x.CrossRefPubMed

126.

Park J, Lee H, Lee S, Lee H. Interventions on reducing exposure to Endocrine Disrupting Chemicals in Human Health Care Context: a scoping review. Risk Manag Healthc Policy. 2022;15:779–91. https://doi.org/10.2147/RMHP.S358561.CrossRefPubMedPubMedCentral

127.

Valvi D, Oulhote Y, Weihe P, et al. Gestational diabetes and offspring birth size at elevated environmental pollutant exposures. Environ Int. 2017;107:205–15. https://doi.org/10.1016/j.envint.2017.07.016.CrossRefPubMedPubMedCentral

128.

Kim J, Sun Q, Yue Y, et al. 4,4’-Dichlorodiphenyltrichloroethane (DDT) and 4,4’-dichlorodiphenyldichloroethylene (DDE) promote adipogenesis in 3T3-L1 adipocyte cell culture. Pestic Biochem Physiol. 2016;131:40–5. https://doi.org/10.1016/j.pestbp.2016.01.005.CrossRefPubMed

129.

Crews D, Gillette R, Scarpino SV, Manikkam M, Savenkova MI, Skinner MK. Epigenetic transgenerational inheritance of altered stress responses. Proc Natl Acad Sci U S A. 2012;109(23):9143–8. https://doi.org/10.1073/pnas.1118514109.CrossRefPubMedPubMedCentral

130.

Wang X, Weng Y, Geng S, et al. Maternal procymidone exposure has lasting effects on murine gut-liver axis and glucolipid metabolism in offspring. Food Chem Toxicol. 2023;174:113657. https://doi.org/10.1016/j.fct.2023.113657.CrossRefPubMed

131.

Wolf C, Lambright C, Mann P, et al. Administration of potentially antiandrogenic pesticides (procymidone, linuron, iprodione, chlozolinate, p,p’-DDE, and ketoconazole) and toxic substances (dibutyl- and diethylhexyl phthalate, PCB 169, and ethane dimethane sulphonate) during sexual differentiation produces diverse profiles of reproductive malformations in the male rat. Toxicol Ind Health. 1999;15(1–2):94–118. https://doi.org/10.1177/074823379901500109.CrossRefPubMed

132.

Migeot V, Albouy-Llaty M, Carles C, et al. Drinking-water exposure to a mixture of nitrate and low-dose atrazine metabolites and small-for-gestational age (SGA) babies: a historic cohort study. Environ Res. 2013;122:58–64. https://doi.org/10.1016/j.envres.2012.12.007.CrossRefPubMed

133.

Goodyer CG, Poon S, Aleksa K, et al. A case-control study of maternal polybrominated diphenyl ether (PBDE) exposure and cryptorchidism in Canadian populations. Environ Health Perspect. 2017;125(5):057004. https://doi.org/10.1289/EHP522.CrossRefPubMedPubMedCentral

134.

Doucet J, Tague B, Arnold DL, Cooke GM, Hayward S, Goodyer CG. Persistent organic pollutant residues in human fetal liver and placenta from Greater Montreal, Quebec: a longitudinal study from 1998 through 2006. Environ Health Perspect. 2009;117(4):605–10. https://doi.org/10.1289/ehp.0800205.CrossRefPubMed

135.

Wang PW, Chen ML, Huang LW, Yang W, Wu KY, Huang YF. Prenatal nonylphenol exposure, oxidative and nitrative stress, and birth outcomes: a cohort study in Taiwan. Environ Pollut. 2015;207:145–51. https://doi.org/10.1016/j.envpol.2015.08.044.CrossRefPubMed

136.

Tsai MS, Chang CH, Tsai YA, et al. Neonatal outcomes of intrauterine nonylphenol exposure–a longitudinal cohort study in Taiwan. Sci Total Environ. 2013;458–460:367–73. https://doi.org/10.1016/j.scitotenv.2013.04.039.CrossRefPubMed

137.

Zheng D, Huo M, Li B, et al. The role of exosomes and Exosomal MicroRNA in Cardiovascular Disease. Front Cell Dev Biol. 2021;8. https://doi.org/10.3389/fcell.2020.616161.

138.

Cao Y, Jia YJ, Xing B, Shi D, Xiang D. Plasma microRNA-16‐5p, ‐17‐5p and ‐20a‐5p: novel diagnostic biomarkers for gestational diabetes mellitus. J Obstet Gynecol Res. 2017;43(6):974–81. https://doi.org/10.1111/jog.13317.CrossRef

139.

Tryggestad JB, Vishwanath A, Jiang S, et al. Influence of gestational diabetes mellitus on human umbilical vein endothelial cell miRNA. Clin Sci. 2016;130(21):1955–67. https://doi.org/10.1042/cs20160305.CrossRef

140.

Ye Z, Wang S, Huang X, et al. Plasma exosomal MIRNAs associated with metabolism as early predictor of gestational diabetes mellitus. Diabetes. 2022;71(11):2272–83. https://doi.org/10.2337/db21-0909.CrossRefPubMedPubMedCentral

141.

Sørensen AE, Van Poppel M, Desoyé G, et al. The temporal Profile of circulating miRNAs during Gestation in overweight and obese women with or without gestational diabetes Mellitus. Biomedicines. 2022;10(2):482. https://doi.org/10.3390/biomedicines10020482.CrossRefPubMedPubMedCentral

142.

Rani PR, Begum J. Screening and diagnosis of gestational diabetes Mellitus, where do we stand. J Clin Diagn Res. 2016;10(4):QE01–4. https://doi.org/10.7860/JCDR/2016/17588.7689.CrossRefPubMedPubMedCentral

Title: Endocrine disrupting chemicals: gestational diabetes and beyond
Authors: Tridip Mitra
Richa Gulati
Krithika Ramachandran
Rohan Rajiv
Elizabeth Ann L. Enninga
Chris K Pierret
Sajeetha Kumari R
Rajiv Janardhanan
Publication date: 01-12-2024
Publisher: BioMed Central
Keywords: Gestational Diabetes
Gestational Diabetes
Epigenetics
Insulins
Insulins
Obesity
Obesity
Published in: Diabetology & Metabolic Syndrome / Issue 1/2024
Electronic ISSN: 1758-5996
DOI: https://doi.org/10.1186/s13098-024-01317-9

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