2023, Número 09
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Ginecol Obstet Mex 2023; 91 (09)
Diabetes materna y deficiencia de zinc: riesgos para la descendencia
Gómez HT, Bequer ML, Clapés HS
Idioma: Español
Referencias bibliográficas: 61
Paginas: 669-678
Archivo PDF: 243.71 Kb.
RESUMEN
Antecedentes: Cuando la mujer embarazada tiene déficit de zinc, esta carencia
puede ser un factor que contribuya a la aparición de alteraciones en el feto, como las
malformaciones congénitas y otros trastornos del desarrollo.
Objetivo: Identificar los aspectos relevantes del estado actual del conocimiento de las
complicaciones de la diabetes en la mujer embarazada y el déficit de zinc en el feto.
Además, explicar cuál es la posible consecuencia de la deficiencia del micronutriente,
entre otras causas moleculares subyacentes.
Metodología: Revisión bibliográfica efectuada en las bases de datos de Google,
PubMed-Medline y SciELO de artículos publicados en inglés o español del año 2012 al
2022, con los MeSH: Maternal diabetes; Hyperglycemia; Zinc deficiency; Congenital
malformations; Epigenetics; con su correspondiente traducción al español. Criterios de
selección: artículos originales, estudios prospectivos, de revisión bibliográfica, metanálisis,
capítulos de libro y reportes de la Asociación Americana de Diabetes (ADA) y
la Asociación Latinoamericana de Diabetes (ALAD).
Resultados: Se localizaron 187 artículos de los que se excluyeron 126 no adecuados
para el tema de la revisión, duplicados o en idioma diferente al inglés y español.
Conclusiones: El análisis bibliográfico evidenció que los trastornos metabólicos
provocados por la hiperglucemia de la madre, el déficit de zinc, la alteración de su
homeostasis y su interacción con el desequilibrio redox, la inflamación de bajo grado,
la activación apoptósica y las modificaciones epigenéticas producen un ambiente
intrauterino adverso que condiciona la aparición de malformaciones y otros trastornos
del desarrollo en la descendencia.
REFERENCIAS (EN ESTE ARTÍCULO)
Brajkovich IE, Aschner P, Taboada L, Camperos P, et al.Consenso ALAD. Tratamiento del paciente con diabetesmellitus tipo 2 y obesidad. Revista ALAD 2019; 9.https://doi.org/10.24875/ALAD.19000369
ALAD. Asociación Latinoamericana de Diabetes. GuíasALAD sobre el diagnóstico, control y tratamiento de ladiabetes mellitus tipo 2 con medicina basada en evidencia.Revista ALAD 2019; https://www.revistaalad.com/guias/5600AX191_guias_alad_2019.pdf
ADA. American Diabetes Association. Classificationand diagnosis of diabetes: Standards of medical care indiabetes. Diabetes Care 2022; 45 (Suppl 1): S17-S38.https://doi.org/10.2337/dc21-S
Silva CM, Arnegard ME, Maric-Bilkan C. Dysglycemiain pregnancy and maternal/fetal outcomes. J WomensHealth 2021; 30 (2): 187-93. https://doi.org/10.1089/jwh.2020.8853
5Rodas W, Mawyin AE, Gómez JL, Rodríguez CV, etal. Diabetes gestacional: fisiopatología, diagnóstico,tratamiento y nuevas perspectivas. Arch Venez deFarmacol y Ter 2018; 37 (3). https://www.redalyc.org/journal/559/55963208008/55963208008.pdf
Rashid CS, Bansal A, Simmons RA. Oxidative stress,intrauterine growth restriction, and developmentalprogramming of type 2 diabetes. Physiology2018; 33(5):248-59. https://doi.org/10.1152/physiol.00023.2018
Vigil P, Olmedo J. Diabetes gestacional: conceptosactuales. Ginecol Obstet Mex 2017; 85 (6): https://ginecologiayobstetricia.org.mx/download/1120
Moore LE. Fetal and neonatal consequences of maternaldiabetes. 2018. In: Diabetes in Pregnancy Texas: Springer.https://cpncampus.com/biblioteca/files/original/ed769533711e833a0436440659637ad7.pdf.
Zabihi S, Loeken MR. Understanding diabetic teratogenesis:Where are we now and where are we going? BirthDefects Res A Clin Mol Teratol 2018; 88 (10): 779-90.https://doi.org/10.1002/bdra.20704
Eletri L, Mitanchez D. How do the different types ofmaternal diabetes during pregnancy influence offspringoutcomes? Nutrients 2022; 14 (3870). https://doi.org/10.3390/nu14183870
Kumar SD, Vijaya M, Samy RP, Dheen ST, et al. Zincsupplementation prevents cardiomyocyte apoptosis andcongenital heart defects in embryos of diabetic mice.Free Radic Biol Med 2012; 53 (8): 1595-606. https://doi.org/10.1016/j.freeradbiomed.2012.07.008
Negrato CA, Marques PR, Leite HB, Torigoe CN, et al.Glycemic and nonglycemic mechanisms of congenitalmalformations in hyperglycemic pregnancies: a narrativereview. Archives of Endocrinology and Metabolism2022; 66 (6): 908-18. https://doi.org/10.20945/2359-3997000000521
Li H, Zhang J, Niswander L. Zinc deficiency causesneural tube defects through attenuation of p53ubiquitylation. Development 2018; 45. https://doi.org/10.1242/dev.169797
Castellón D, Garcia M, Bequer L, Freire C, et al. Efectosobre el peso fetal de la suplementación con zinc a ratasdiabéticas gestadas. Medicent Elecrón 2022; 26 (3).http://www.medicentro.sld.cu/index.php/medicentro/article/view/3504/2956
Iqbal S, Ali I. Effect of maternal zinc supplementation orzinc status on pregnancy complications and perinataloutcomes: An umbrella review of meta-analyses. Heliyon2021; 7 (7). https://doi.org/10.1016/j.heliyon.2021.e07540
1Shams AS, Mohammed MH, Loka MM, Abdel RahmanGM. Assessment of the protective role of prenatal zincversus insulin supplementation on fetal cardiac damageinduced by maternal diabetes in rat using caspase-3and KI67 immunohistochemical stains. Cardiol ResPract 2016. http://dx.doi.org/10.1155/2016/7469549
Çelikel OO, Doğan O, Aksoy N. A multilateral investigationof the effects of zinc level on pregnancy. J ClinLab Anal 2018; 32. https://doi.org/10.1002/jcla.22398
Taboada N, Mollineda A, Herrera M. Serum copper,zinc, calcium and magnesium levels in mothers withoffspring affected by neural tube defects: a case-controlstudy. Rev Cuba de Investig Biomed 2019; 38 (1). https://www.medigraphic.com/pdfs/revcubinvbio/cib-2019/cib191g.pdf
Demirtas MS. The pathogenesis of congenital anomalies:Roles of teratogens and infections. In: Verma RP,editor. Congenital anomalies in newborn infants. London: IntechOpen 2020; 57-83. https://doi.org/10.5772/intechopen.92580
Garner TB, Hester JM, Carothers A, Diaz FJ. Role ofzinc in female reproduction. Biol Reprod 2021; 104(5): 976-94. https://doi.org/10.1093/biolre/ioab023
Mendes F, Gobetto MN, Casta A, Lucero D, et al.Fetal and postnatal zinc restriction: Sex differences inmetabolic alterations in adult rats. Nutrition 2019; 65(1): 18-26. https://doi.org/10.1016/j.nut.2019.01.022
Wilson RL, Leemaqz SY, Goh Z, McAninch D, et al.Zinc is a critical regulator of placental morphogenesisand aternal hemodynamics during pregnancy in mice.Sci Rep 2017; 7 (1): 1-14. https://doi.org/10.1038/s41598-017-15085-2
Fukunaka A, Fujitani Y. Role of zinc homeostasis in thepathogenesis of diabetes and obesity. Int J Mol Sci 2018;19. https://doi.org/10.3390/ijms19020476
Lawson R, Maret W, Hogstrand C. ZnT8 haploinsuffiencyimpacts MIN6 cell zinc content and -cell phenotypevia ZIP-ZnT8 coregulation. Int J Mol Sci 2019; 20.https://doi.org/10.3390/ijms20215485
MacKenzie S, Bergdahl A. Zinc homeostasis in diabetesmellitus and vascular complications. Biomedicines2022; 10. https://doi.org/10.3390/biomedicines10010139
Norouzi S, Adulcikas J, Sohal SS, Myers S. Zinc stimulatesglucose oxidation and glycemic control bymodulating the insulin signaling pathway in humanand mouse skeletal muscle cell lines. PLoS One 2018;13.https://doi.org/10.1371/journal.pone.0191727
Huang L, Tepaamorndech S, Kirschke CP, Newman JW,et al. Aberrant fatty acid metabolism in skeletal musclecontributes to insulin resistance in zinc transporter 7 (Znt7)-knockout mice. Biol Chem 2018; 293 (20): 7549-63. https://doi.org/10.1074/jbc.M117.817692
Norouzi S, Adulcikas J, Henstridge D, Sonda S, et al. Thezinc transporter Zip7 is downregulated in skeletal muscleof insulin-resistant cells and in mice fed a high-fat diet.Cells 2019; 8. https://doi.org/10.3390/cells8070663
Huang Q, Du J, Merriman C, Gong Z. Genetic,functional, and immunological study of ZnT8in diabetes. Int J Endocrinol 2019. https://doi.org/10.1155/2019/1524905
Ullah R, Shehzad A, Shah MA, March M, et al. CTerminaldomain of the human zinc transporter hZnT8is structurally indistinguishable from its disease riskvariant (R325W). Int J Mol Sci 2020; 21. http://www.mdpi.com/1422-0067/21/3/926
Prabhakar SM. Linkage of a plasma zinc signature andimpaired insulin receptor activation: Implications for themechanism of type 2 diabetes mellitus. bioRxiv 2019.https://doi.org/10.1101/849091
Poudel RR, Bhusal Y, Tharu B, Kafle NK. Roleof zinc in insulin regulation and diabetes. J SocHealth Diabetes 2017; 5 (1): 83-7. https://doi.org/10.1055/s-0038-1676241
Gómez T, Bequer L, Mollineda A, Molina JL, et al.Concentration of zinc, copper, iron, calcium andmagnesium in the serum, tissues and urine of streptozotocin-induced mild-diabetic rat model. Biol TraceElem Res 2017; 179: 237-46. https://doi.org/10.1007/s12011-017-0962-x
Villota D, Casillas M, Morales MP, Farías M, MayagoitiaC. Desenlace materno-fetal en pacientes condiagnóstico temprano o tardío de diabetes gestacional.Ginecol Obstet Mex 2019; 87 (12): 785-91. https://doi.org/10.24245/gom.v87i12.3255
Ornoy A, Reece EA, Pavlinkova G, Kappen C, et al.Effect of maternal diabetes on the embryo, fetus, andchildren: Congenital anomalies, genetic and epigeneticchanges and developmental outcomes. Birth DefectsRes 2015; 105 (1): 53-72. https://doi.org/10.1002/bdrc.21090
Bhandari J, Thada PK, Khattar D. Diabetic embryopathy.Treasure Island (FL): StatPearls Publishing; 2022. https://europepmc.org/article/nbk/nbk558974#free-full-text.
Modzelewski R, Stefanowicz-Rutkowska MM, MatuszewskiW, Bandurska-Stankiewicz EM. Gestationaldiabetes mellitus. Recent literature review. Clin Med2022; 11 (19). https://doi.org/10.3390/jcm11195736
Jawerbaum A, White V. Review on intrauterine programming:Consequences in rodent models of milddiabetes and mild fat overfeeding are not mild. Placenta2017; 52 (1): 21-32. https://doi.org/10.1016/j.placenta.2017.02.009
Ogunsola O, Arikawe A, Iranloye B, Adegoke O. Maternalserum progesterone levels and placental expressionof progesterone receptors in insulin-resistant pregnantrats. J Afr Ass Physiol Sci 2019; 7 (2). https://www.ajol.info/index.php/jaaps/article/view/192648
Dela-Justina V, San-Martin S, López-Espíndola D, BressanA, Alves de Freitas R, Lopes de Passos AM, et al.Increased expression of STAT3 and SOCS3 in placentafrom hyperglycemic rats. Eur J Histochem 2019; 63 (4):222-28. https://doi.org/10.4081/ejh.2019.3054
Clapés S, Fernández T, Suárez G. Oxidative stress andbirth defects in infants of women with pregestationaldiabtes. Medicc Review 2013; 15 (1): 37-40. https://doi.org/10.37757/MR2013V15.N1.9
Moore LE. Preconception counseling. 2018. In:Diabetes in Pregnancy Texas: Springer InternationalPublishing AG. https://cpncampus.com/biblioteca/files/original/ed769533711e833a0436440659637ad7.pdf.
Gómez T, García M, Bequer L, Freire C, Aimee VilaM, Clapés C. Malformaciones esqueléticas y alteracionesdel crecimiento en fetos de ratas con diabetesmoderada. Biomédica 2021; 41 (3): 1-7. https://doi.org/10.7705/biomedica.5736
Castori M. Diabetic embryopathy: A developmentalperspective from fertilization to adulthood.Mol Syndromol 2013; 4 (2): 74-86. https://doi.org/10.1159/000345205
Clapés S, Fernández T, Prado K. El desafío para el desarrollodel sistema nervioso central en la reproducciónhumana asociada con la diabetes. Revista Cubana deEndocrinología 2022; 33 (1). http://www.revendocrinologia.sld.cu/index.php/endocrinologia/article/view/310
Wang X, Lu J, Xie W, Lu X, Liang Y, Li M, et al.Maternal diabetes induces autism-like behavior byhyperglycemia-mediated persistent oxidative stressand suppression of superoxide dismutase 2. Proc NatlAcad Sci USA 2019; 116 (47): 23743-52. https://doi.org/10.1073/pnas.1912625116
Khamis A, Canouil M, Keikkala E, Hummel S, Bonnefond,A, Delahaye F, et al. Both gestational diabetesexposure and maternal methylome interaction impactoffspring epigenetic signature. Diabet 2021; 9 (1): 34-36. https://emj.emg-health.com/wp-content/uploads/sites/2/2021/11/Both-Gestational-Diabetes-Exposureand-Maternal-Methylome-Interaction-Impact-Offspring-Epigenetic-Signature.pdf
Bequer L, Gómez T, Molina J, Álvarez A, et al. Experimentaldiabetes impairs maternal reproductive performancein pregnant Wistar rats and their offspring. SystBiol Reprod Med 2018; 64 (1): 7. https://doi.org/10.1080/19396368.2017.1395928
Gatti CR, Roberti SL, Capobianco E, Gómez D, et al.Decidual abnormalities in the prepubertal period and atday 9 of pregnancy in diabetic rat offspring. Univ Med2020; 2020. https://revistas.javeriana.edu.co/index.php/vnimedica/article/view/31046
Gómez T, Bequer L, Mollineda A, González O, et al.Serum zinc levels of cord blood: Relation to birth weightand gestational period. J Trace Elem Med Biol 2015; 30:180-3. http://dx.doi.org/10.1016/j.jtemb.2014.12.009
Mendes F, Caniffi C, Arranz CT, Tomat AL. Impact ofzinc deficiency during prenatal and/or postnatal life oncardiovascular and metabolic diseases: Experimentaland clinical evidence. Adv Nutr 2022; 13 (3): 833-45.https://doi.org/10.1093/advances/nmac012
Juriol LV, Gobetto MN, Mendes F, Dasso ME, et al.Cardiac changes in apoptosis, inflammation, oxidativestress, and nitric oxide system induced by prenatal andpostnatal zinc deficiency in male and female rats. EurJ Nutr 2016; 57 (2): 569-83. http://doi.org/10.1007/s00394-016-1343-5
Adamo AM, Liu X, Mathieu P, Nuttall JR, et al. Earlydevelopmental marginal zinc deficiency affects neurogenesisdecreasing neuronal number and alteringneuronal specification in the adult rat brain. Front CellNeurosci 2019; 13 (62): 52-63. https://doi.org/10.3389/fncel.2019.00062
Choi S, Hong DK, Choi BY, Suh WS. Zinc in the brain:Friend or foe? Int J Mol Sci 2020; 21. https://doi.org/10.3390/ijms21238941
Zuccarello D, Sorrentino U, Brasson V, Marin L, et al.Epigenetics of pregnancy: looking beyond the DNAcode. J Assist Reprod Genet 2022; 39: 801-16. https://doi.org/10.1007/s10815-022-02451-x
Higa R, Leonardi ML, Jawerbaum A. Intrauterineprogramming of cardiovascular diseases in maternaldiabetes. Diabetes Front Physiol 2021; 12. https://doi.org/10.3389/fphys.2021.760251
Brito S, Lee M, Bin B, Lee J. Zinc and its transportersin epigenetics. Mol Cells 2020; 43 (4): 323-30. https://doi.org/10.14348/molcells.2020.0026
Seman NA, Mohamud WN, Östenson C, Brismar K, etal. Increased DNA methylation of the SLC30A8 genepromoter is associated with type 2 diabetes in a Malaypopulation. Clin Epigenetics 2015; 7 (1): 15-30. https://doi.org/10.1186/s13148-015-0049-5
Yusuf AP, Abubakar MB, Malami I, Ibrahim KG, et al.Zinc metalloproteins in epigenetics and their crosstalk.Life Sci 2021; 11 (3): 186. https://doi.org/10.3390/life11030186
Tiffon C. The impact of nutrition and environmentalepigenetics on human health and disease. Int J MolSci 2018; 19. https://doi.org/10.3390/ijms19113425
Zhang Y, Kutateladze TG. Diet and the epigenome.Nat Commun 2018; 9: 3375. https://doi.org/10.1038/s41467-018-05778-1