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Diabetologia

Erschienen in:

27.08.2019 | Review

Environmental neglect: endocrine disruptors as underappreciated but potentially modifiable diabetes risk factors

verfasst von: Robert M. Sargis, Rebecca A. Simmons

Erschienen in: Diabetologia | Ausgabe 10/2019

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Abstract

Type 2 diabetes prevalence is increasing dramatically across the globe, imposing a tremendous toll on individuals and healthcare systems. Reversing these trends requires comprehensive approaches to address both classical and emerging diabetes risk factors. Recently, environmental toxicants acting as endocrine-disrupting chemicals (EDCs) have emerged as novel metabolic disease risk factors. EDCs implicated in diabetes pathogenesis include various inorganic and organic molecules of both natural and synthetic origin, including arsenic, bisphenol A, phthalates, polychlorinated biphenyls and organochlorine pesticides. Indeed, evidence implicates EDC exposures across the lifespan in metabolic dysfunction; moreover, specific developmental windows exhibit enhanced sensitivity to EDC-induced metabolic disruption, with potential impacts across generations. Importantly, differential exposures to diabetogenic EDCs likely also contribute to racial/ethnic and economic disparities. Despite these emerging links, clinical practice guidelines fail to address this underappreciated diabetes risk factor. Comprehensive approaches to stem the tide of diabetes must include efforts to address its environmental drivers.

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International Diabetes Federation (2017) IDF Diabetes Atlas, 8th Edition. Available from www.idf.org/e-library/epidemiology-research/diabetes-atlas/134-idf-diabetes-atlas-8th-edition.html. Accessed 15 Jan 2018

World Health Organization (2016) Global report on diabetes. World Health Organization, Geneva

American Diabetes Association (2018) Economic costs of diabetes in the U.S. in 2017. Diabetes Care 41(5):917–928. https://doi.org/10.2337/dci18-0007 CrossRefPubMedCentral

Squires E, Duber H, Campbell M et al (2018) Health care spending on diabetes in the U.S., 1996-2013. Diabetes Care 41(7):1423–1431. https://doi.org/10.2337/dc17-1376 CrossRefPubMedPubMedCentral

Gore AC, Chappell VA, Fenton SE et al (2015) EDC-2: the Endocrine Society’s second scientific statement on endocrine-disrupting chemicals. Endocr Rev 36(6):E1–E150. https://doi.org/10.1210/er.2015-1010 CrossRefPubMedPubMedCentral

Zoeller RT, Brown TR, Doan LL et al (2012) Endocrine-disrupting chemicals and public health protection: a statement of principles from the Endocrine Society. Endocrinology 153(9):4097–4110. https://doi.org/10.1210/en.2012-1422 CrossRefPubMedPubMedCentral

Heindel JJ, Blumberg B, Cave M et al (2017) Metabolism disrupting chemicals and metabolic disorders. Reprod Toxicol 68:3–33. https://doi.org/10.1016/j.reprotox.2016.10.001 CrossRefPubMed

Mimoto MS, Nadal A, Sargis RM (2017) Polluted pathways: mechanisms of metabolic disruption by endocrine disrupting chemicals. Curr Environ Health Rep 4(2):208–222. https://doi.org/10.1007/s40572-017-0137-0 CrossRefPubMedPubMedCentral

Sargis RM (2014) The hijacking of cellular signaling and the diabetes epidemic: mechanisms of environmental disruption of insulin action and glucose homeostasis. Diabetes Metab J 38(1):1–12. https://doi.org/10.4093/dmj.2014.38.1.1 CrossRef

10.

Neel BA, Sargis RM (2011) The paradox of progress: environmental disruption of metabolism and the diabetes epidemic. Diabetes 60(7):1838–1848. https://doi.org/10.2337/db11-0153 CrossRefPubMedPubMedCentral

11.

Tuduri E, Marroqui L, Dos Santos RS, Quesada I, Fuentes E, Alonso-Magdalena P (2019) Timing of exposure to bisphenol-A: implications for diabetes development. Front Endocrinol (Lausanne) 9:648. https://doi.org/10.3389/fendo.2018.00648 CrossRef

12.

Calafat AM, Ye X, Wong LY, Reidy JA, Needham LL (2008) Exposure of the U.S. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Environ Health Perspect 116(1):39–44. https://doi.org/10.1289/ehp.10753 CrossRefPubMed

13.

Ikezuki Y, Tsutsumi O, Takai Y, Kamei Y, Taketani Y (2002) Determination of bisphenol A concentrations in human biological fluids reveals significant early prenatal exposure. Hum Reprod 17(11):2839–2841. https://doi.org/10.1093/humrep/17.11.2839 CrossRefPubMed

14.

Schonfelder G, Wittfoht W, Hopp H, Talsness CE, Paul M, Chahoud I (2002) Parent bisphenol A accumulation in the human maternal-fetal-placental unit. Environ Health Perspect 110(11):A703–A707. https://doi.org/10.1289/ehp.110-1241091 CrossRefPubMedPubMedCentral

15.

Nahar MS, Liao C, Kannan K, Dolinoy DC (2013) Fetal liver bisphenol A concentrations and biotransformation gene expression reveal variable exposure and altered capacity for metabolism in humans. J Biochem Mol Toxicol 27(2):116–123. https://doi.org/10.1002/jbt.21459 CrossRefPubMed

16.

Vom Saal FS, Nagel SC, Coe BL, Angle BM, Taylor JA (2012) The estrogenic endocrine disrupting chemical bisphenol A (BPA) and obesity. Mol Cell Endocrinol 354(1–2):74–84. https://doi.org/10.1016/j.mce.2012.01.001 CrossRefPubMedPubMedCentral

17.

Susiarjo M, Xin F, Bansal A et al (2015) Bisphenol A exposure disrupts metabolic health across multiple generations in the mouse. Endocrinology 156(6):2049–2058. https://doi.org/10.1210/en.2014-2027 CrossRefPubMedPubMedCentral

18.

Bansal A, Rashid C, Xin F et al (2017) Sex- and dose-specific effects of maternal bisphenol A exposure on pancreatic islets of first- and second-generation adult mice offspring. Environ Health Perspect 125(9):097022. https://doi.org/10.1289/EHP1674 CrossRefPubMedPubMedCentral

19.

Bansal A, Li C, Xin F, et al. (2018) Transgenerational effects of maternal bisphenol: a exposure on offspring metabolic health. J Dev Orig Health Dis 1–12. https://doi.org/10.1017/S2040174418000764

20.

Rubin BS, Schaeberle CM, Soto AM (2019) The case for BPA as an obesogen: contributors to the controversy. Front Endocrinol (Lausanne) 10:30. https://doi.org/10.3389/fendo.2019.00030 CrossRef

21.

Rubin BS, Murray MK, Damassa DA, King JC, Soto AM (2001) Perinatal exposure to low doses of bisphenol A affects body weight, patterns of estrous cyclicity, and plasma LH levels. Environ Health Perspect 109(7):675–680. https://doi.org/10.1289/ehp.01109675 CrossRefPubMedPubMedCentral

22.

Tiano JP, Mauvais-Jarvis F (2012) Importance of oestrogen receptors to preserve functional beta-cell mass in diabetes. Nat Rev Endocrinol 8(6):342–351. https://doi.org/10.1038/nrendo.2011.242 CrossRefPubMed

23.

Whitehead R, Guan H, Arany E, Cernea M, Yang K (2016) Prenatal exposure to bisphenol A alters mouse fetal pancreatic morphology and islet composition. Horm Mol Biol Clin Invest 25(3):171–179. https://doi.org/10.1515/hmbci-2015-0052 CrossRef

24.

Garcia-Arevalo M, Alonso-Magdalena P, Rebelo Dos Santos J, Quesada I, Carneiro EM, Nadal A (2014) Exposure to bisphenol-A during pregnancy partially mimics the effects of a high-fat diet altering glucose homeostasis and gene expression in adult male mice. PLoS One 9(6):e100214. https://doi.org/10.1371/journal.pone.0100214 CrossRefPubMedPubMedCentral

25.

Garcia-Arevalo M, Alonso-Magdalena P, Servitja JM et al (2016) Maternal exposure to bisphenol-A during pregnancy increases pancreatic beta-cell growth during early life in male mice offspring. Endocrinology 157(11):4158–4171. https://doi.org/10.1210/en.2016-1390 CrossRefPubMed

26.

Chamorro-Garcia R, Diaz-Castillo C, Shoucri BM et al (2017) Ancestral perinatal obesogen exposure results in a transgenerational thrifty phenotype in mice. Nat Commun 8(1):2012. https://doi.org/10.1038/s41467-017-01944-z CrossRefPubMedPubMedCentral

27.

Veiga-Lopez A, Pu Y, Gingrich J, Padmanabhan V (2018) Obesogenic endocrine disrupting chemicals: identifying knowledge gaps. Trends Endocrinol Metab 29(9):607–625. https://doi.org/10.1016/j.tem.2018.06.003 CrossRefPubMedPubMedCentral

28.

Mennigen JA, Thompson LM, Bell M, Tellez Santos M, Gore AC (2018) Transgenerational effects of polychlorinated biphenyls: 1. Development and physiology across 3 generations of rats. Environ Health 17(1):18. https://doi.org/10.1186/s12940-018-0362-5 CrossRefPubMedPubMedCentral

29.

Skinner MK (2016) Endocrine disruptors in 2015: epigenetic transgenerational inheritance. Nat Rev Endocrinol 12(2):68–70. https://doi.org/10.1038/nrendo.2015.206 CrossRefPubMed

30.

Drobna Z, Henriksen AD, Wolstenholme JT et al (2018) Transgenerational effects of bisphenol A on gene expression and DNA methylation of imprinted genes in brain. Endocrinology 159(1):132–144. https://doi.org/10.1210/en.2017-00730 CrossRefPubMed

31.

Chamorro-Garcia R, Sahu M, Abbey RJ, Laude J, Pham N, Blumberg B (2013) Transgenerational inheritance of increased fat depot size, stem cell reprogramming, and hepatic steatosis elicited by prenatal exposure to the obesogen tributyltin in mice. Environ Health Perspect 121(3):359–366. https://doi.org/10.1289/ehp.1205701 CrossRefPubMedPubMedCentral

32.

Ptak A, Gregoraszczuk EL (2012) Bisphenol A induces leptin receptor expression, creating more binding sites for leptin, and activates the JAK/Stat, MAPK/ERK and PI3K/Akt signalling pathways in human ovarian cancer cell. Toxicol Lett 210(3):332–337. https://doi.org/10.1016/j.toxlet.2012.02.003 CrossRefPubMed

33.

Xu X, Lu Y, Zhang G et al (2014) Bisphenol A promotes dendritic morphogenesis of hippocampal neurons through estrogen receptor-mediated ERK1/2 signal pathway. Chemosphere 96:129–137. https://doi.org/10.1016/j.chemosphere.2013.09.063 CrossRefPubMed

34.

Acconcia F, Pallottini V, Marino M (2015) Molecular mechanisms of action of BPA. Dose Response 13(4):1559325815610582. https://doi.org/10.1177/1559325815610582 CrossRefPubMedPubMedCentral

35.

Fernandez MF, Arrebola JP, Jimenez-Diaz I et al (2016) Bisphenol A and other phenols in human placenta from children with cryptorchidism or hypospadias. Reprod Toxicol 59:89–95. https://doi.org/10.1016/j.reprotox.2015.11.002 CrossRefPubMed

36.

Prasanth GK, Divya LM, Sadasivan C (2010) Bisphenol-A can bind to human glucocorticoid receptor as an agonist: an in silico study. J Appl Toxicol 30(8):769–774. https://doi.org/10.1002/jat.1570 CrossRefPubMed

37.

Sargis RM, Johnson DN, Choudhury RA, Brady MJ (2010) Environmental endocrine disruptors promote adipogenesis in the 3T3-L1 cell line through glucocorticoid receptor activation. Obesity 18(7):1283–1288. https://doi.org/10.1038/oby.2009.419 CrossRefPubMed

38.

Wang J, Sun B, Hou M, Pan X, Li X (2013) The environmental obesogen bisphenol A promotes adipogenesis by increasing the amount of 11β-hydroxysteroid dehydrogenase type 1 in the adipose tissue of children. Int J Obes 37(7):999–1005. https://doi.org/10.1038/ijo.2012.173 CrossRef

39.

Somm E, Schwitzgebel VM, Toulotte A et al (2009) Perinatal exposure to bisphenol A alters early adipogenesis in the rat. Environ Health Perspect 117(10):1549–1555. https://doi.org/10.1289/ehp.11342 CrossRefPubMedPubMedCentral

40.

Riu A, Grimaldi M, le Maire A et al (2011) Peroxisome proliferator-activated receptor gamma is a target for halogenated analogs of bisphenol A. Environ Health Perspect 119(9):1227–1232. https://doi.org/10.1289/ehp.1003328 CrossRefPubMedPubMedCentral

41.

Grun F, Watanabe H, Zamanian Z et al (2006) Endocrine-disrupting organotin compounds are potent inducers of adipogenesis in vertebrates. Mol Endocrinol 20(9):2141–2155. https://doi.org/10.1210/me.2005-0367 CrossRefPubMed

42.

Shoucri BM, Hung VT, Chamorro-Garcia R, Shioda T, Blumberg B (2018) Retinoid X receptor activation during adipogenesis of female mesenchymal stem cells programs a dysfunctional adipocyte. Endocrinology 159(8):2863–2883. https://doi.org/10.1210/en.2018-00056 CrossRefPubMedPubMedCentral

43.

Regnier SM, El-Hashani E, Kamau W, Zhang X, Massad NL, Sargis RM (2015) Tributyltin differentially promotes development of a phenotypically distinct adipocyte. Obesity 23(9):1864–1871. https://doi.org/10.1002/oby.21174 CrossRefPubMed

44.

Jiang Y, Xia W, Zhu Y et al (2014) Mitochondrial dysfunction in early life resulted from perinatal bisphenol A exposure contributes to hepatic steatosis in rat offspring. Toxicol Lett 228(2):85–92. https://doi.org/10.1016/j.toxlet.2014.04.013 CrossRefPubMed

45.

Chandravanshi LP, Gupta R, Shukla RK (2018) Developmental neurotoxicity of arsenic: involvement of oxidative stress and mitochondrial functions. Biol Trace Elem Res 186(1):185–198. https://doi.org/10.1007/s12011-018-1286-1 CrossRefPubMed

46.

Dolinoy DC, Huang D, Jirtle RL (2007) Maternal nutrient supplementation counteracts bisphenol A-induced DNA hypomethylation in early development. Proc Natl Acad Sci U S A 104(32):13056–13061. https://doi.org/10.1073/pnas.0703739104 CrossRefPubMedPubMedCentral

47.

Tindula G, Murphy SK, Grenier C et al (2018) DNA methylation of imprinted genes in Mexican-American newborn children with prenatal phthalate exposure. Epigenomics 10(7):1011–1026. https://doi.org/10.2217/epi-2017-0178 CrossRefPubMedPubMedCentral

48.

Pogribny IP, Tryndyak VP, Boureiko A et al (2008) Mechanisms of peroxisome proliferator-induced DNA hypomethylation in rat liver. Mutat Res 644(1–2):17–23. https://doi.org/10.1016/j.mrfmmm.2008.06.009 CrossRefPubMedPubMedCentral

49.

Meakin CJ, Martin EM, Szilagyi JT, Nylander-French LA, Fry RC (2019) Inorganic arsenic as an endocrine disruptor: modulation of the glucocorticoid receptor pathway in placental cells via CpG methylation. Chem Res Toxicol 32(3):493–499. https://doi.org/10.1021/acs.chemrestox.8b00352 CrossRefPubMed

50.

Bellavia A, Chiu YH, Brown FM et al (2019) Urinary concentrations of parabens mixture and pregnancy glucose levels among women from a fertility clinic. Environ Res 168:389–396. https://doi.org/10.1016/j.envres.2018.10.009 CrossRefPubMed

51.

Ouyang F, Tang N, Zhang HJ et al (2018) Maternal urinary triclosan level, gestational diabetes mellitus and birth weight in Chinese women. Sci Total Environ 626:451–457. https://doi.org/10.1016/j.scitotenv.2018.01.102 CrossRefPubMedPubMedCentral

52.

Shaffer RM, Ferguson KK, Sheppard L et al (2019) Maternal urinary phthalate metabolites in relation to gestational diabetes and glucose intolerance during pregnancy. Environ Int 123:588–596. https://doi.org/10.1016/j.envint.2018.12.021 CrossRefPubMedPubMedCentral

53.

Ashley-Martin J, Dodds L, Arbuckle TE et al (2018) Association between maternal urinary speciated arsenic concentrations and gestational diabetes in a cohort of Canadian women. Environ Int 121(Pt 1):714–720. https://doi.org/10.1016/j.envint.2018.10.008 CrossRefPubMed

54.

Xia X, Liang C, Sheng J et al (2018) Association between serum arsenic levels and gestational diabetes mellitus: a population-based birth cohort study. Environ Pollut 235:850–856. https://doi.org/10.1016/j.envpol.2018.01.016 CrossRefPubMed

55.

Marie C, Leger S, Guttmann A et al (2018) Exposure to arsenic in tap water and gestational diabetes: a French semi-ecological study. Environ Res 161:248–255. https://doi.org/10.1016/j.envres.2017.11.016 CrossRefPubMed

56.

Farzan SF, Gossai A, Chen Y, Chasan-Taber L, Baker E, Karagas M (2016) Maternal arsenic exposure and gestational diabetes and glucose intolerance in the New Hampshire birth cohort study. Environ Health 15(1):106. https://doi.org/10.1186/s12940-016-0194-0 CrossRefPubMedPubMedCentral

57.

Shapiro GD, Dodds L, Arbuckle TE et al (2015) Exposure to phthalates, bisphenol A and metals in pregnancy and the association with impaired glucose tolerance and gestational diabetes mellitus: the MIREC study. Environ Int 83:63–71. https://doi.org/10.1016/j.envint.2015.05.016 CrossRefPubMed

58.

Munoz MP, Valdes M, Munoz-Quezada MT et al (2018) Urinary inorganic arsenic concentration and gestational diabetes mellitus in pregnant women from Arica, Chile. Int J Environ Res Public Health 15(7). https://doi.org/10.3390/ijerph15071418

59.

Alonso-Magdalena P, Vieira E, Soriano S et al (2010) Bisphenol A exposure during pregnancy disrupts glucose homeostasis in mothers and adult male offspring. Environ Health Perspect 118(9):1243–1250. https://doi.org/10.1289/ehp.1001993 CrossRefPubMedPubMedCentral

60.

Alonso-Magdalena P, Garcia-Arevalo M, Quesada I, Nadal A (2015) Bisphenol-A treatment during pregnancy in mice: a new window of susceptibility for the development of diabetes in mothers later in life. Endocrinology 156(5):1659–1670. https://doi.org/10.1210/en.2014-1952 CrossRefPubMed

61.

Maull EA, Ahsan H, Edwards J et al (2012) Evaluation of the association between arsenic and diabetes: a National Toxicology Program workshop review. Environ Health Perspect 120(12):1658–1670. https://doi.org/10.1289/ehp.1104579 CrossRefPubMedPubMedCentral

62.

Sung TC, Huang JW, Guo HR (2015) Association between arsenic exposure and diabetes: a meta-analysis. Biomed Res Int 2015:368087–368010. https://doi.org/10.1155/2015/368087 CrossRefPubMedPubMedCentral

63.

Wang W, Xie Z, Lin Y, Zhang D (2014) Association of inorganic arsenic exposure with type 2 diabetes mellitus: a meta-analysis. J Epidemiol Community Health 68(2):176–184. https://doi.org/10.1136/jech-2013-203114 CrossRefPubMed

64.

Ranciere F, Lyons JG, Loh VH et al (2015) Bisphenol A and the risk of cardiometabolic disorders: a systematic review with meta-analysis of the epidemiological evidence. Environ Health 14(1):46. https://doi.org/10.1186/s12940-015-0036-5 CrossRefPubMedPubMedCentral

65.

Song Y, Chou EL, Baecker A et al (2016) Endocrine-disrupting chemicals, risk of type 2 diabetes, and diabetes-related metabolic traits: a systematic review and meta-analysis. J Diabetes 8(4):516–532. https://doi.org/10.1111/1753-0407.12325 CrossRefPubMed

66.

Jensen TK, Timmermann AG, Rossing LI et al (2014) Polychlorinated biphenyl exposure and glucose metabolism in 9-year-old Danish children. J Clin Endocrinol Metab 99(12):E2643–E2651. https://doi.org/10.1210/jc.2014-1683 CrossRefPubMedPubMedCentral

67.

Suarez-Lopez JR, Lee DH, Porta M, Steffes MW, Jacobs DR Jr (2015) Persistent organic pollutants in young adults and changes in glucose related metabolism over a 23-year follow-up. Environ Res 137:485–494. https://doi.org/10.1016/j.envres.2014.11.001 CrossRefPubMedPubMedCentral

68.

Tang M, Chen K, Yang F, Liu W (2014) Exposure to organochlorine pollutants and type 2 diabetes: a systematic review and meta-analysis. PLoS One 9(10):e85556. https://doi.org/10.1371/journal.pone.0085556 CrossRefPubMedPubMedCentral

69.

Taylor KW, Novak RF, Anderson HA et al (2013) Evaluation of the association between persistent organic pollutants (POPs) and diabetes in epidemiological studies: a national toxicology program workshop review. Environ Health Perspect 121(7):774–783. https://doi.org/10.1289/ehp.1205502 CrossRefPubMedPubMedCentral

70.

Shoshtari-Yeganeh B, Zarean M, Mansourian M et al (2019) Systematic review and meta-analysis on the association between phthalates exposure and insulin resistance. Environ Sci Pollut Res Int 26(10):9435–9442. https://doi.org/10.1007/s11356-019-04373-1 CrossRefPubMed

71.

Sun Q, Cornelis MC, Townsend MK et al (2014) Association of urinary concentrations of bisphenol a and phthalate metabolites with risk of type 2 diabetes: a prospective investigation in the Nurses’ Health Study (NHS) and NHSII cohorts. Environ Health Perspect 122(6):616–623. https://doi.org/10.1289/ehp.1307201 CrossRefPubMedPubMedCentral

72.

Lind PM, Zethelius B, Lind L (2012) Circulating levels of phthalate metabolites are associated with prevalent diabetes in the elderly. Diabetes Care 35(7):1519–1524. https://doi.org/10.2337/dc11-2396 CrossRefPubMedPubMedCentral

73.

Rajesh P, Sathish S, Srinivasan C, Selvaraj J, Balasubramanian K (2013) Phthalate is associated with insulin resistance in adipose tissue of male rat: role of antioxidant vitamins. J Cell Biochem 114(3):558–569. https://doi.org/10.1002/jcb.24399 CrossRefPubMed

74.

Indumathi D, Jayashree S, Selvaraj J et al (2013) Effect of bisphenol-A on insulin signal transduction and glucose oxidation in skeletal muscle of adult male albino rat. Hum Exp Toxicol 32(9):960–971. https://doi.org/10.1177/0960327112470273 CrossRefPubMed

75.

Jayashree S, Indumathi D, Akilavalli N, Sathish S, Selvaraj J, Balasubramanian K (2013) Effect of bisphenol-A on insulin signal transduction and glucose oxidation in liver of adult male albino rat. Environ Toxicol Pharmacol 35(2):300–310. https://doi.org/10.1016/j.etap.2012.12.016 CrossRefPubMed

76.

Han JC, Park SY, Hah BG et al (2003) Cadmium induces impaired glucose tolerance in rat by down-regulating GLUT4 expression in adipocytes. Arch Biochem Biophys 413(2):213–220. https://doi.org/10.1016/S0003-9861(03)00120-6 CrossRefPubMed

77.

Liu PC, Matsumura F (1995) Differential effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin on the "adipose- type" and "brain-type" glucose transporters in mice. Mol Pharmacol 47(1):65–73PubMed

78.

Enan E, Matsumura F (1994) 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD)-induced changes in glucose transporting activity in guinea pigs, mice, and rats in vivo and in vitro. J Biochem Toxicol 9(2):97–106. https://doi.org/10.1002/jbt.2570090207 CrossRefPubMed

79.

Regnier SM, Kirkley AG, Ruiz D et al (2018) Diet-dependence of metabolic perturbations mediated by the endocrine disruptor tolylfluanid. Endocr Connect 7(1):159–168. https://doi.org/10.1530/EC-17-0320 CrossRefPubMed

80.

Regnier SM, Kirkley AG, Ye H et al (2015) Dietary exposure to the endocrine disruptor tolylfluanid promotes global metabolic dysfunction in male mice. Endocrinology 156(3):896–910. https://doi.org/10.1210/en.2014-1668 CrossRefPubMed

81.

Paul DS, Walton FS, Saunders RJ, Styblo M (2011) Characterization of the impaired glucose homeostasis produced in C57BL/6 mice by chronic exposure to arsenic and high-fat diet. Environ Health Perspect 119(8):1104–1109. https://doi.org/10.1289/ehp.1003324 CrossRefPubMedPubMedCentral

82.

Kirkley AG, Carmean CM, Ruiz D et al (2018) Arsenic exposure induces glucose intolerance and alters global energy metabolism. Am J Physiol Regul Integr Comp Physiol 314(2):R294–R303. https://doi.org/10.1152/ajpregu.00522.2016 CrossRefPubMed

83.

Hill DS, Wlodarczyk BJ, Mitchell LE, Finnell RH (2009) Arsenate-induced maternal glucose intolerance and neural tube defects in a mouse model. Toxicol Appl Pharmacol 239(1):29–36. https://doi.org/10.1016/j.taap.2009.05.009 CrossRefPubMedPubMedCentral

84.

Sun Q, Yue P, Deiuliis JA et al (2009) Ambient air pollution exaggerates adipose inflammation and insulin resistance in a mouse model of diet-induced obesity. Circulation 119(4):538–546. https://doi.org/10.1161/CIRCULATIONAHA.108.799015 CrossRefPubMed

85.

Panahi P, Vosough-Ghanbari S, Pournourmohammadi S et al (2006) Stimulatory effects of malathion on the key enzymes activities of insulin secretion in langerhans islets, glutamate dehydrogenase and glucokinase. Toxicol Mech Methods 16(4):161–167. https://doi.org/10.1080/15376520500191623 CrossRefPubMed

86.

Batista TM, Alonso-Magdalena P, Vieira E et al (2012) Short-term treatment with bisphenol-a leads to metabolic abnormalities in adult male mice. PLoS One 7(3):e33814. https://doi.org/10.1371/journal.pone.0033814 CrossRefPubMedPubMedCentral

87.

Zuo Z, Chen S, Wu T et al (2011) Tributyltin causes obesity and hepatic steatosis in male mice. Environ Toxicol 26(1):79–85. https://doi.org/10.1002/tox.20531 CrossRefPubMed

88.

Huang CF, Yang CY, Chan DC et al (2015) Arsenic exposure and glucose intolerance/insulin resistance in estrogen-deficient female mice. Environ Health Perspect 123(11):1138–1144. https://doi.org/10.1289/ehp.1408663 CrossRefPubMedPubMedCentral

89.

Lim S, Ahn SY, Song IC et al (2009) Chronic exposure to the herbicide, atrazine, causes mitochondrial dysfunction and insulin resistance. PLoS One 4(4):e5186. https://doi.org/10.1371/journal.pone.0005186 CrossRefPubMedPubMedCentral

90.

Moon MK, Jeong IK, Jung Oh T et al (2015) Long-term oral exposure to bisphenol A induces glucose intolerance and insulin resistance. J Endocrinol 226(1):35–42. https://doi.org/10.1530/JOE-14-0714 CrossRefPubMed

91.

Baker NA, Karounos M, English V et al (2013) Coplanar polychlorinated biphenyls impair glucose homeostasis in lean C57BL/6 mice and mitigate beneficial effects of weight loss on glucose homeostasis in obese mice. Environ Health Perspect 121(1):105–110. https://doi.org/10.1289/ehp.1205421 CrossRefPubMed

92.

Gray SL, Shaw AC, Gagne AX, Chan HM (2013) Chronic exposure to PCBs (Aroclor 1254) exacerbates obesity-induced insulin resistance and hyperinsulinemia in mice. J Toxicol Environ Health A 76(12):701–715. https://doi.org/10.1080/15287394.2013.796503 CrossRefPubMed

93.

Huang CF, Yang CY, Tsai JR, Wu CT, Liu SH, Lan KC (2018) Low-dose tributyltin exposure induces an oxidative stress-triggered JNK-related pancreatic beta-cell apoptosis and a reversible hypoinsulinemic hyperglycemia in mice. Sci Rep 8(1):5734. https://doi.org/10.1038/s41598-018-24076-w CrossRefPubMedPubMedCentral

94.

Sargis RM (2015) Metabolic disruption in context: clinical avenues for synergistic perturbations in energy homeostasis by endocrine disrupting chemicals. Endocrine Disruptors 3(1):e1080788-1080781-1080787. https://doi.org/10.1080/23273747.2015.1080788 CrossRef

95.

Wei J, Lin Y, Li Y et al (2011) Perinatal exposure to bisphenol A at reference dose predisposes offspring to metabolic syndrome in adult rats on a high-fat diet. Endocrinology 152(8):3049–3061. https://doi.org/10.1210/en.2011-0045 CrossRefPubMed

96.

Ding S, Fan Y, Zhao N et al (2014) High-fat diet aggravates glucose homeostasis disorder caused by chronic exposure to bisphenol A. J Endocrinol 221(1):167–179. https://doi.org/10.1530/JOE-13-0386 CrossRefPubMed

97.

La Merrill M, Karey E, Moshier E et al (2014) Perinatal exposure of mice to the pesticide DDT impairs energy expenditure and metabolism in adult female offspring. PLoS One 9(7):e103337. https://doi.org/10.1371/journal.pone.0103337 CrossRefPubMedPubMedCentral

98.

Wan HT, Zhao YG, Leung PY, Wong CK (2014) Perinatal exposure to perfluorooctane sulfonate affects glucose metabolism in adult offspring. PLoS One 9(1):e87137. https://doi.org/10.1371/journal.pone.0087137 CrossRefPubMedPubMedCentral

99.

Strakovsky RS, Lezmi S, Shkoda I, Flaws JA, Helferich WG, Pan YX (2015) In utero growth restriction and catch-up adipogenesis after developmental di (2-ethylhexyl) phthalate exposure cause glucose intolerance in adult male rats following a high-fat dietary challenge. J Nutr Biochem 26(11):1208–1220. https://doi.org/10.1016/j.jnutbio.2015.05.012 CrossRefPubMedPubMedCentral

100.

Howell GE 3rd, Mulligan C, Meek E, Chambers JE (2015) Effect of chronic p,p'-dichlorodiphenyldichloroethylene (DDE) exposure on high fat diet-induced alterations in glucose and lipid metabolism in male C57BL/6H mice. Toxicology 328:112–122. https://doi.org/10.1016/j.tox.2014.12.017 CrossRefPubMed

101.

Baker NA, Shoemaker R, English V et al (2015) Effects of adipocyte aryl hydrocarbon receptor deficiency on PCB-induced disruption of glucose homeostasis in lean and obese mice. Environ Health Perspect 123(10):944–950. https://doi.org/10.1289/ehp.1408594 CrossRefPubMedPubMedCentral

102.

Dirtu AC, Dirinck E, Malarvannan G et al (2013) Dynamics of organohalogenated contaminants in human serum from obese individuals during one year of weight loss treatment. Environ Sci Technol 47(21):12441–12449. https://doi.org/10.1021/es400657t CrossRefPubMed

103.

Dirinck E, Dirtu AC, Jorens PG, Malarvannan G, Covaci A, Van Gaal LF (2015) Pivotal role for the visceral fat compartment in the release of persistent organic pollutants during weight loss. J Clin Endocrinol Metab 100(12):4463–4471. https://doi.org/10.1210/jc.2015-2571 CrossRefPubMed

104.

Hue O, Marcotte J, Berrigan F et al (2006) Increased plasma levels of toxic pollutants accompanying weight loss induced by hypocaloric diet or by bariatric surgery. Obes Surg 16(9):1145–1154. https://doi.org/10.1381/096089206778392356 CrossRefPubMed

105.

Charlier C, Desaive C, Plomteux G (2002) Human exposure to endocrine disrupters: consequences of gastroplasty on plasma concentration of toxic pollutants. Int J Obes Relat Metab Disord 26(11):1465–1468. https://doi.org/10.1038/sj.ijo.0802144 CrossRefPubMed

106.

Beckles GL, Chou CF, Centers for Disease Control and Prevention (CDC) (2013) Diabetes - United States, 2006 and 2010. MMWR Surveill Summ 62(3):99–104

107.

Ferdinand KC, Nasser SA (2015) Racial/ethnic disparities in prevalence and care of patients with type 2 diabetes mellitus. Curr Med Res Opin 31(5):913–923. https://doi.org/10.1185/03007995.2015.1029894 CrossRefPubMed

108.

Peek ME (2011) Gender differences in diabetes-related lower extremity amputations. Clin Orthop Relat Res 469(7):1951–1955. https://doi.org/10.1007/s11999-010-1735-4 CrossRefPubMed

109.

Nsiah-Kumi P, Ortmeier SR, Brown AE (2009) Disparities in diabetic retinopathy screening and disease for racial and ethnic minority populations—a literature review. J Natl Med Assoc 101(5):430–437. https://doi.org/10.1016/S0027-9684(15)30929-9 CrossRefPubMed

110.

Rosenstock S, Whitman S, West JF, Balkin M (2014) Racial disparities in diabetes mortality in the 50 most populous US cities. J Urban Health 91(5):873–885. https://doi.org/10.1007/s11524-013-9861-4 CrossRefPubMedPubMedCentral

111.

Ruiz D, Becerra M, Jagai JS, Ard K, Sargis RM (2018) Disparities in environmental exposures to endocrine-disrupting chemicals and diabetes risk in vulnerable populations. Diabetes Care 41(1):193–205. https://doi.org/10.2337/dc16-2765 CrossRefPubMed

112.

Trasande L, Spanier AJ, Sathyanarayana S, Attina TM, Blustein J (2013) Urinary phthalates and increased insulin resistance in adolescents. Pediatrics 132(3):e646–e655. https://doi.org/10.1542/peds.2012-4022 CrossRefPubMedPubMedCentral

113.

Huang T, Saxena AR, Isganaitis E, James-Todd T (2014) Gender and racial/ethnic differences in the associations of urinary phthalate metabolites with markers of diabetes risk: National Health and Nutrition Examination Survey 2001-2008. Environ Health 13(1):6. https://doi.org/10.1186/1476-069X-13-6 CrossRefPubMedPubMedCentral

114.

Di Q, Wang Y, Zanobetti A et al (2017) Air pollution and mortality in the medicare population. N Engl J Med 376(26):2513–2522. https://doi.org/10.1056/NEJMoa1702747 CrossRefPubMedPubMedCentral

115.

American Diabetes Association (2019) Standards of medical care in diabetes: 2019. Diabetes Care 42(Suppl 1):S1–S186. https://doi.org/10.2337/dc19-S001 CrossRef

116.

Sargis RM, Heindel JJ, Padmanabhan V (2019) Interventions to address environmental metabolism-disrupting chemicals: changing the narrative to empower action to restore metabolic health. Front Endocrinol (Lausanne) 10:33. https://doi.org/10.3389/fendo.2019.00033 CrossRef

117.

Vogelmeier CF, Criner GJ, Martinez FJ et al (2017) Global strategy for the diagnosis, management, and prevention of chronic obstructive lung disease 2017 report. GOLD executive summary. Am J Respir Crit Care Med 195(5):557–582. https://doi.org/10.1164/rccm.201701-0218PP CrossRefPubMed

118.

National Asthma Education Prevention Program (2007) Expert Panel Report 3 (EPR-3): Guidelines for the Diagnosis and Management of Asthma-Summary Report 2007. J Allergy Clin Immunol 120(5 Suppl):94–138. https://doi.org/10.1016/j.jaci.2007.09.043 CrossRef

119.

Wang B, Xu D, Jing Z, Liu D, Yan S, Wang Y (2014) Effect of long-term exposure to air pollution on type 2 diabetes mellitus risk: a systemic review and meta-analysis of cohort studies. Eur J Endocrinol 171(5):R173–R182. https://doi.org/10.1530/EJE-14-0365 CrossRefPubMed

120.

Zhao Z, Lin F, Wang B, Cao Y, Hou X, Wang Y (2016) Residential proximity to major roadways and risk of type 2 diabetes mellitus: a meta-analysis. Int J Environ Res Public Health 14(1). https://doi.org/10.3390/ijerph14010003

121.

Di Renzo GC, Conry JA, Blake J et al (2015) International Federation of Gynecology and Obstetrics opinion on reproductive health impacts of exposure to toxic environmental chemicals. Int J Gynaecol Obstet 131(3):219–225. https://doi.org/10.1016/j.ijgo.2015.09.002 CrossRefPubMedPubMedCentral

122.

American College of Obstetricians and Gynecologists (2013) Exposure to toxic environmental agents. Fertil Steril 100(4):931–934. https://doi.org/10.1016/j.fertnstert.2013.08.043 CrossRef

123.

Legler J, Fletcher T, Govarts E et al (2015) Obesity, diabetes, and associated costs of exposure to endocrine-disrupting chemicals in the European Union. J Clin Endocrinol Metab 100(4):1278–1288. https://doi.org/10.1210/jc.2014-4326 CrossRefPubMedPubMedCentral

124.

Trasande L, Lampa E, Lind L, Lind PM (2017) Population attributable risks and costs of diabetogenic chemical exposures in the elderly. J Epidemiol Community Health 71(2):111–114. https://doi.org/10.1136/jech-2016-208006 CrossRefPubMed

125.

Shaikh S, Jagai JS, Ashley C, Zhou S, Sargis RM (2018) Underutilized and under threat: environmental policy as a tool to address diabetes risk. Curr Diab Rep 18(5):25. https://doi.org/10.1007/s11892-018-0993-5 CrossRefPubMedPubMedCentral

126.

Vandenberg LN, Maffini MV, Sonnenschein C, Rubin BS, Soto AM (2009) Bisphenol-A and the great divide: a review of controversies in the field of endocrine disruption. Endocr Rev 30(1):75–95. https://doi.org/10.1210/er.2008-0021 CrossRefPubMedPubMedCentral

127.

Stahlhut RW, Myers JP, Taylor JA, Nadal A, Dyer JA, Vom Saal FS (2018) Experimental BPA exposure and glucose-stimulated insulin response in adult men and women. J Endocr Soc 2(10):1173–1187. https://doi.org/10.1210/js.2018-00151 CrossRefPubMedPubMedCentral

128.

Hagobian TA, Bird A, Stanelle S, Williams D, Schaffner A, Phelan S (2019) Pilot study on the effect of orally administered bisphenol A on glucose and insulin response in nonobese adults. J Endocr Soc 3(3):643–654. https://doi.org/10.1210/js.2018-00322 CrossRefPubMedPubMedCentral

129.

Kahn SE, Hull RL, Utzschneider KM (2006) Mechanisms linking obesity to insulin resistance and type 2 diabetes. Nature 444(7121):840–846. https://doi.org/10.1038/nature05482 CrossRefPubMed

Titel: Environmental neglect: endocrine disruptors as underappreciated but potentially modifiable diabetes risk factors
verfasst von: Robert M. Sargis
Rebecca A. Simmons
Publikationsdatum: 27.08.2019
Verlag: Springer Berlin Heidelberg
Erschienen in: Diabetologia / Ausgabe 10/2019
Print ISSN: 0012-186X
Elektronische ISSN: 1432-0428
DOI: https://doi.org/10.1007/s00125-019-4940-z

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