<?xml version="1.0" encoding="ISO-8859-1"?><article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
<front>
<journal-meta>
<journal-id>0300-9041</journal-id>
<journal-title><![CDATA[Ginecología y obstetricia de México]]></journal-title>
<abbrev-journal-title><![CDATA[Ginecol. obstet. Méx.]]></abbrev-journal-title>
<issn>0300-9041</issn>
<publisher>
<publisher-name><![CDATA[Federación Mexicana de Colegios de Obstetricia y Ginecología A.C.]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S0300-90412023000900006</article-id>
<article-id pub-id-type="doi">10.24245/gom.v91i9.8385</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Diabetes materna y deficiencia de zinc: riesgos para la descendencia]]></article-title>
<article-title xml:lang="en"><![CDATA[Maternal diabetes and zinc deficiency, risks for the offspring.]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Gómez Hernández]]></surname>
<given-names><![CDATA[Tahiry]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Bequer Mendoza]]></surname>
<given-names><![CDATA[Leticia]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Clapés Hernández]]></surname>
<given-names><![CDATA[Sonia]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Universidad de Ciencias Médicas de Villa Clara Unidad de Investigaciones Biomédicas ]]></institution>
<addr-line><![CDATA[La Habana ]]></addr-line>
<country>Cuba</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,Universidad de Ciencias Médicas de Villa Clara Unidad de Investigaciones Biomédicas ]]></institution>
<addr-line><![CDATA[La Habana ]]></addr-line>
<country>Cuba</country>
</aff>
<aff id="Af3">
<institution><![CDATA[,Universidad de Ciencias Médicas de La Habana  ]]></institution>
<addr-line><![CDATA[ ]]></addr-line>
<country>Cuba</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>00</month>
<year>2023</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>00</month>
<year>2023</year>
</pub-date>
<volume>91</volume>
<numero>9</numero>
<fpage>669</fpage>
<lpage>678</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_arttext&amp;pid=S0300-90412023000900006&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_abstract&amp;pid=S0300-90412023000900006&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_pdf&amp;pid=S0300-90412023000900006&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[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.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract  BACKGROUND: When pregnant women are deficient in zinc, this deficiency may be a contributing factor to foetal disorders, such as congenital malformations and other developmental disorders.  OBJECTIVE:  To identify the relevant aspects of the current state of knowledge of the complications of diabetes in pregnant women and zinc deficiency in the foetus. In addition, to explain the possible consequences of micronutrient deficiency, among other underlying molecular causes.  METHODOLOGY: Bibliographic review carried out in Google, PubMed-Medline and SciELO databases of articles published in English or Spanish from 2012 to 2022, with the MeSH: Maternal diabetes; Hyperglycemia; Zinc deficiency; Congenital malformations; Epigenetics; with their corresponding translation into Spanish. Selection criteria: original articles, prospective studies, literature reviews, meta-analyses, book chapters and reports of the American Diabetes Association (ADA) and the Latin American Diabetes Association (ALAD).  RESULTS: 187 articles were located of which 126 unsuitable for the review topic, duplicates or in language other than English and Spanish were excluded.  CONCLUSIONS: The literature review evidenced that metabolic disorders caused by maternal hyperglycemia, zinc deficiency, alteration of its homeostasis and its interaction with redox imbalance, low-grade inflammation, apoptotic activation and epigenetic modifications produce an adverse intrauterine environment that conditions the appearance of malformations and other developmental disorders in the offspring.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[Zinc]]></kwd>
<kwd lng="es"><![CDATA[diabetes en el embarazo]]></kwd>
<kwd lng="es"><![CDATA[factores de riesgo]]></kwd>
<kwd lng="es"><![CDATA[malformaciones congénitas]]></kwd>
<kwd lng="es"><![CDATA[estrés oxidativo]]></kwd>
<kwd lng="es"><![CDATA[epigenética]]></kwd>
<kwd lng="en"><![CDATA[Zinc]]></kwd>
<kwd lng="en"><![CDATA[Pregnancy in Diabetics]]></kwd>
<kwd lng="en"><![CDATA[Risk Factors]]></kwd>
<kwd lng="en"><![CDATA[Abnormalities]]></kwd>
<kwd lng="en"><![CDATA[Oxidative Stress]]></kwd>
<kwd lng="en"><![CDATA[Epigenetic]]></kwd>
</kwd-group>
</article-meta>
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