Palabras clave
disruptores endocrinos
diabetes mellitus tipo 1
diabetes mellitus tipo 2
dibutil ftalato
fitoestrógenos
obesidad
parabenos
diabetes mellitus tipo 1
diabetes mellitus tipo 2
dibutil ftalato
fitoestrógenos
obesidad
parabenos
Cómo citar
Sánchez, P., Zanabria, M., Latorre, S., Calvache, J., Coy, A., & Rojas, W. (2020). Disruptores endocrinos y su camino hacia el desequilibrio metabólico. Revista Colombiana De Endocrinología, Diabetes &Amp; Metabolismo, 7(1), 38–42. https://doi.org/10.53853/encr.7.1.567
Resumen
El presente artículo de revisión tiene como objetivo presentar, de forma resumida, la evidencia que existe sobre las repercusiones metabólicas a nivel de obesidad y diabetes, que se genera como consecuencia de la exposición a sustancias químicas exógenas, denominadas disruptores endocrinos (DE), a las cuales nos exponemos de forma cotidiana y que afectan nuestra salud y la de nuestra descendencia. Adicionalmente, con la presente revisión hacemos un llamado no solo a la comunidad médica, sino a los sectores involucrados en la producción, distribución y reglamentación del uso de estas sustancias, pues cada vez hay más evidencia de los efectos nocivos que pueden generar y debemos evitar su uso.
Los datos se obtuvieron de estudios clínicos aleatorizados y de una revisión en idioma español e inglés de los últimos 15 años, que incluyó los términos DeCS: disruptores endocrinos, con alternativa DeCS: sustancias disruptoras endocrinas y efecto disruptor endocrino, así como términos MeSH: endocrine disruptors y alternativas MeSH: disruptors, endocrine; endocrine disrupting chemicals; chemicals, endocrine disrupting; endocrine disruptor effect; disruptor effect, endocrine; effect, endocrine disruptor; endocrine disruptor effects; disruptor effects, endocrine; effects, endocrine disruptor.
Citas
1. Bergman Å, Heindel J, Kasten T, Kidd K, Jobling S, Neira M, et al. The impact of endocrine disruption: a consensus statement on the state of the science. Environ Health Perspect. 2013;121(4):A104-6.
2. Zoeller R, Brown T, Doan L, Gore A, Skakkebaek N, Soto A, et al. Endocrinedisrupting chemicals and public health protection: a statement of principles from the Endocrine Society. Endocrinology. 2012;153(9):4097-110.
3. Ferre P. The biology of peroxisome proliferator-activated receptors. Diabetes. 2004;53(1):S43-50.
4. Janesick A, Blumberg B. Minireview: PPAR? as the target of obesogens. J Steroid Biochem Mol Biol. 2011;127(1-2):4-8.
5. Kim HK, Nelson-Dooley C, Della-Fera M, Yang JY, Zhang W, Duan J, et al. Genistein decreases food intake, body weight, and fat pad weight and causes adipose tissue apoptosis in ovariectomized female mice. J Nutr. 2006;136(2):409-14.
6. Wu J, Oka J, Tabata I, Higuchi M, Toda T, Fuku N, et al. Effects of isoflavone and exercise on BMD and fat mass in postmenopausal Japanese women: a 1-year randomized placebo-controlled trial. J Bone Miner Res. 2006.
7. Ruhlen R, Howdeshell K, Mao J, Taylor J, Bronson F, Newbold R, et al. Low phytoestrogen levels in feed increase fetal serum estradiol resulting in the “fetal estrogenization syndrome” and obesity in CD-1 mice. Environ Health Perspect. 2008;116;3:322-8.
8. Domazet SL, Grontved A, Timmermann AG, Nielsen F, Jensen TK. Longitudinal associations of exposure to perfluoroalkylated substances in childhood and adolescence and indicators of adiposity and glucose metabolism 6 and 12 years later: the European youth heart study. Diabetes Care. 2016;39(10):1745-51.
9. Rönn M, Lind L, Örberg J, Kullberg J, Söderberg S, Larsson A, et al. Bisphenol A is related to circulating levels of adiponectin, leptin and ghrelin, but not to fat mass or fat distribution in humans. Chemosphere. 2014;112:42-8.
10. Liu G, Dhana K, Furtado J, Rood J, Zong G, Liang L, et al. Perfluoroalkyl substances and changes in body weight and resting metabolic rate in response to weight-loss diets: a prospective study. PLoS Med. 2018;13;15(2):e1002502.
11. Paolella G, Burgos Aceves M, Lionetti L, Di Gregorio I, Busiello R, Lepretti M. Environmental pollutants effect on brown adipose tissue. Front Physiol. 2019;9:1-8.
12. Gore A, Chappell V, Fenton S, Flaws J, Nadal A, Prins G, et al. The endocrine society’s second scientific statement on endocrine-disrupting chemicals. Endocr Rev. 2015;36(6):E1-E150.
13. Bodin J, Stene L, Nygaard U. Can exposure to environmental chemicals increase the risk of diabetes type 1 development? Biomed Res Int. 2015;208947:19.
14. Howard S, Lee D. What is the role of human contamination by environmental chemicals in the development of type 1 diabetes? J Epidemiol Community Health. 2012;66(6):479-81.
15. Eze I, Hemkens L, Bucher H, Hoffmann B, Schindler C, Künzli N, et al. Association between ambient air pollution and diabetes mellitus in Europe and North America: systematic review and meta-analysis. Environ Health Perspect. 2015;123(5):381-9.
16. Bodin J, Bølling A, Becher R, Kuper F, Løvik M, Nygaard U. Transmaternal bisphenol an exposure accelerates diabetes type 1 development in NOD mice. Toxicol Sci. 2014;137(2):311-23.
17. Bodin J, Groeng E, Andreassen M, Dirven H, Nygaard U. Exposure to perfluoroundecanoic acid (PFUnDA) accelerates insulitis development in a mouse model of type 1 diabetes. Toxicol Reports. 2016; 29;3:664-72.
18. Grau-Pérez M, Kuo C, Spratlen M, Thayer K, Mendez M, Hamman R, et al. The association of arsenic exposure and metabolism with type 1 and type 2 diabetes in youth: the search case-control study. Diabetes Care. 2017;40(1):46-53.
19. Xu J, Huang G, Guo T. Developmental bisphenol A exposure modulates immune-related diseases. Toxics. 2016;26;4(4).
20. Dahlquist G. Can we slow the rising incidence of childhood-onset autoimmune diabetes? The overload hypothesis. Diabetologia. 2006;49(1):20-4.
21. Ahn C, Kang H, Lee J, Hong E, Jung E, Yoo Y, et al. Bisphenol A and octylphenol exacerbate type 1 diabetes mellitus by disrupting calcium homeostasis in mouse pancreas. Toxicol Lett. 2018;295:162-72.
22. Debost-Legrand A, Warembourg C, Massart C, Chevrier C, Bonvallot N, Monfort C, et al. Prenatal exposure to persistent organic pollutants and organophosphate pesticides, and markers of glucose metabolism at birth. Environ Res. 2016;146:207-17.
23. Sant K, Jacobs H, Borofski K, Moss J, Timme-Laragy A. Embryonic exposures to perfluorooctanesulfonic acid (PFOS) disrupt pancreatic organogenesis in the zebrafish, Danio rerio. Environ Pollut. 2017;220(B):807-17.
24. Sant K, Jacobs H, Xu J, Borofski K, Moss L, Moss J, et al. Assessment of toxicological perturbations and variants of pancreatic islet development in the zebrafish model. Toxics. 2016;4(3): pii: 20.
25. Bodin J, Kocbach Bølling A, Wendt A, Eliasson L, Becher R, Kuper F, et al. Exposure to bisphenol A, but not phthalates, increases spontaneous diabetes type 1 development in NOD mice. Toxicol Reports. 2015;2:99-110.
26. Sakkiah S, Wang T, Zou W, Wang Y, Pan B, Tong W, et al. Endocrine disrupting chemicals mediated through binding androgen receptor are associated with diabetes mellitus. Int J Environ Res Public Health. 2017;15(1):25.
27. Ruiz D, Becerra M, Jagai J, Ard K, Sargis R. Disparities in environmental exposures to endocrine-disrupting chemicals and diabetes risk in vulnerable populations. Diabetes Care. 2018;41(1):193-205.
28. Song Y, Chou EL, Baecker A, You NCY, Song Y, Sun Q, et al. Endocrine-disrupting chemicals, risk of type 2 diabetes, and diabetes-related metabolic traits: a systematic review and meta-analysis. J Diabetes. 2016;8(4):516-32.
29. Bi Y, Wang W, Xu M, Wang T, Lu J, Xu Y, et al. Diabetes genetic risk score modifies effect of bisphenol A exposure on deterioration in glucose metabolism. J Clin Endocrinol Metab. 2016;101(1):143-50.
2. Zoeller R, Brown T, Doan L, Gore A, Skakkebaek N, Soto A, et al. Endocrinedisrupting chemicals and public health protection: a statement of principles from the Endocrine Society. Endocrinology. 2012;153(9):4097-110.
3. Ferre P. The biology of peroxisome proliferator-activated receptors. Diabetes. 2004;53(1):S43-50.
4. Janesick A, Blumberg B. Minireview: PPAR? as the target of obesogens. J Steroid Biochem Mol Biol. 2011;127(1-2):4-8.
5. Kim HK, Nelson-Dooley C, Della-Fera M, Yang JY, Zhang W, Duan J, et al. Genistein decreases food intake, body weight, and fat pad weight and causes adipose tissue apoptosis in ovariectomized female mice. J Nutr. 2006;136(2):409-14.
6. Wu J, Oka J, Tabata I, Higuchi M, Toda T, Fuku N, et al. Effects of isoflavone and exercise on BMD and fat mass in postmenopausal Japanese women: a 1-year randomized placebo-controlled trial. J Bone Miner Res. 2006.
7. Ruhlen R, Howdeshell K, Mao J, Taylor J, Bronson F, Newbold R, et al. Low phytoestrogen levels in feed increase fetal serum estradiol resulting in the “fetal estrogenization syndrome” and obesity in CD-1 mice. Environ Health Perspect. 2008;116;3:322-8.
8. Domazet SL, Grontved A, Timmermann AG, Nielsen F, Jensen TK. Longitudinal associations of exposure to perfluoroalkylated substances in childhood and adolescence and indicators of adiposity and glucose metabolism 6 and 12 years later: the European youth heart study. Diabetes Care. 2016;39(10):1745-51.
9. Rönn M, Lind L, Örberg J, Kullberg J, Söderberg S, Larsson A, et al. Bisphenol A is related to circulating levels of adiponectin, leptin and ghrelin, but not to fat mass or fat distribution in humans. Chemosphere. 2014;112:42-8.
10. Liu G, Dhana K, Furtado J, Rood J, Zong G, Liang L, et al. Perfluoroalkyl substances and changes in body weight and resting metabolic rate in response to weight-loss diets: a prospective study. PLoS Med. 2018;13;15(2):e1002502.
11. Paolella G, Burgos Aceves M, Lionetti L, Di Gregorio I, Busiello R, Lepretti M. Environmental pollutants effect on brown adipose tissue. Front Physiol. 2019;9:1-8.
12. Gore A, Chappell V, Fenton S, Flaws J, Nadal A, Prins G, et al. The endocrine society’s second scientific statement on endocrine-disrupting chemicals. Endocr Rev. 2015;36(6):E1-E150.
13. Bodin J, Stene L, Nygaard U. Can exposure to environmental chemicals increase the risk of diabetes type 1 development? Biomed Res Int. 2015;208947:19.
14. Howard S, Lee D. What is the role of human contamination by environmental chemicals in the development of type 1 diabetes? J Epidemiol Community Health. 2012;66(6):479-81.
15. Eze I, Hemkens L, Bucher H, Hoffmann B, Schindler C, Künzli N, et al. Association between ambient air pollution and diabetes mellitus in Europe and North America: systematic review and meta-analysis. Environ Health Perspect. 2015;123(5):381-9.
16. Bodin J, Bølling A, Becher R, Kuper F, Løvik M, Nygaard U. Transmaternal bisphenol an exposure accelerates diabetes type 1 development in NOD mice. Toxicol Sci. 2014;137(2):311-23.
17. Bodin J, Groeng E, Andreassen M, Dirven H, Nygaard U. Exposure to perfluoroundecanoic acid (PFUnDA) accelerates insulitis development in a mouse model of type 1 diabetes. Toxicol Reports. 2016; 29;3:664-72.
18. Grau-Pérez M, Kuo C, Spratlen M, Thayer K, Mendez M, Hamman R, et al. The association of arsenic exposure and metabolism with type 1 and type 2 diabetes in youth: the search case-control study. Diabetes Care. 2017;40(1):46-53.
19. Xu J, Huang G, Guo T. Developmental bisphenol A exposure modulates immune-related diseases. Toxics. 2016;26;4(4).
20. Dahlquist G. Can we slow the rising incidence of childhood-onset autoimmune diabetes? The overload hypothesis. Diabetologia. 2006;49(1):20-4.
21. Ahn C, Kang H, Lee J, Hong E, Jung E, Yoo Y, et al. Bisphenol A and octylphenol exacerbate type 1 diabetes mellitus by disrupting calcium homeostasis in mouse pancreas. Toxicol Lett. 2018;295:162-72.
22. Debost-Legrand A, Warembourg C, Massart C, Chevrier C, Bonvallot N, Monfort C, et al. Prenatal exposure to persistent organic pollutants and organophosphate pesticides, and markers of glucose metabolism at birth. Environ Res. 2016;146:207-17.
23. Sant K, Jacobs H, Borofski K, Moss J, Timme-Laragy A. Embryonic exposures to perfluorooctanesulfonic acid (PFOS) disrupt pancreatic organogenesis in the zebrafish, Danio rerio. Environ Pollut. 2017;220(B):807-17.
24. Sant K, Jacobs H, Xu J, Borofski K, Moss L, Moss J, et al. Assessment of toxicological perturbations and variants of pancreatic islet development in the zebrafish model. Toxics. 2016;4(3): pii: 20.
25. Bodin J, Kocbach Bølling A, Wendt A, Eliasson L, Becher R, Kuper F, et al. Exposure to bisphenol A, but not phthalates, increases spontaneous diabetes type 1 development in NOD mice. Toxicol Reports. 2015;2:99-110.
26. Sakkiah S, Wang T, Zou W, Wang Y, Pan B, Tong W, et al. Endocrine disrupting chemicals mediated through binding androgen receptor are associated with diabetes mellitus. Int J Environ Res Public Health. 2017;15(1):25.
27. Ruiz D, Becerra M, Jagai J, Ard K, Sargis R. Disparities in environmental exposures to endocrine-disrupting chemicals and diabetes risk in vulnerable populations. Diabetes Care. 2018;41(1):193-205.
28. Song Y, Chou EL, Baecker A, You NCY, Song Y, Sun Q, et al. Endocrine-disrupting chemicals, risk of type 2 diabetes, and diabetes-related metabolic traits: a systematic review and meta-analysis. J Diabetes. 2016;8(4):516-32.
29. Bi Y, Wang W, Xu M, Wang T, Lu J, Xu Y, et al. Diabetes genetic risk score modifies effect of bisphenol A exposure on deterioration in glucose metabolism. J Clin Endocrinol Metab. 2016;101(1):143-50.
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