<?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>0034-7531</journal-id>
<journal-title><![CDATA[Revista Cubana de Pediatría]]></journal-title>
<abbrev-journal-title><![CDATA[Rev Cubana Pediatr]]></abbrev-journal-title>
<issn>0034-7531</issn>
<publisher>
<publisher-name><![CDATA[Centro Nacional de Información de Ciencias MédicasEditorial Ciencias Médicas]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S0034-75312020000100008</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Microbiota intestinal y obesidad en la infancia]]></article-title>
<article-title xml:lang="en"><![CDATA[Gut microbiota and obesity in childhood]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Castañeda Guillot]]></surname>
<given-names><![CDATA[Carlos]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
<xref ref-type="aff" rid="Aaf"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Universidad Regional Autónoma de Los Andes (UNIANDES) Facultad de Ciencias Médicas ]]></institution>
<addr-line><![CDATA[Ambato ]]></addr-line>
<country>Ecuador</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,Universidad de Ciencias Médicas de La Habana Facultad de Medicina Calixto García ]]></institution>
<addr-line><![CDATA[ ]]></addr-line>
<country>Cuba</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>03</month>
<year>2020</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>03</month>
<year>2020</year>
</pub-date>
<volume>92</volume>
<numero>1</numero>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://scielo.sld.cu/scielo.php?script=sci_arttext&amp;pid=S0034-75312020000100008&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://scielo.sld.cu/scielo.php?script=sci_abstract&amp;pid=S0034-75312020000100008&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://scielo.sld.cu/scielo.php?script=sci_pdf&amp;pid=S0034-75312020000100008&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[RESUMEN  Introducción: La obesidad está relacionada con afecciones metabólicas y sistémicas, como la resistencia a la insulina, diabetes mellitus tipo 2, hígado graso no alcohólico, aterosclerosis e hipertensión arterial, mediante la producción de balance energético positivo por aumento del aporte calórico de la dieta y disminución del gasto de energía asociado con baja actividad física, eventos que son su causa principal.  Objetivos: Analizar la participación de la microbiota intestinal en la obesidad y los mecanismos que intervienen en dicho proceso en ratones, los propuestos en humanos y el papel de modulación de la microbiota intestinal como tratamiento.  Métodos: Se revisaron publicaciones en español e inglés en PubMed, Google Scholar, ScIELO, desde enero 2005 a febrero 2019, se usaron los términos: microbiota intestinal, obesidad y modulación microbiota intestinal.  Resultados: se actualizaron los criterios relacionados con la microbiota intestinal y la obesidad, su incremento y repercusión en pediatría. Se revisaron los principales estudios experimentales en ratones y humanos realizados desde el decenio 2001-2010 y eventos en el microbioma como factor patogénico. Se describieron los mecanismos definidos en la microbiota intestinal participantes en la obesidad y se revisaron los argumentos de modulación del intestino para regular las alteraciones producidas en la obesidad.  Consideraciones finales: Se demuestra la participación de la microbiota intestinal como factor predisponente en la fisiopatología de la obesidad y su modulación terapéutica con distintos métodos de bioterapia para restablecer la heterogeneidad del microbioma, entre ellos, son promisorios, el uso de prebióticos, probióticos, simbióticos y el trasplante de microbiota fecal.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[ABSTRACT  Introduction:  Obesity is linked to metabolic and systemic diseases, such as insulin resistance, diabetes mellitus type 2, non-alcoholic fatty liver disease, atherosclerosis and high blood pressure, through the production of positive energy balance by increasing calories intake in the diet and the decrease energy associated with low physical activity; being these events the main cause of obesity.  Objectives:  To analyze the participation of the gut microbiota in obesity and the mechanisms involved in this process in mice, the proposed in humans and the role of modulation of the gut microbiota as a treatment.  Methods:  Publications in English and Spanish on PubMed, Google Scholar, ScIELO from January 2005 to February 2019 were reviewed, and were used the terms: gut microbiota, obesity and modulation of gut microbiota.  Results:  There were updated the criteria related to the gut microbiota and obesity, its increase and impact on pediatrics. The main experimental studies in mice and humans made during the decade 2001-2010 and events in the microbiome as pathogenic factor were reviewed. The mechanisms defined in the gut microbiota which participate in obesity were reviewed, as well as the arguments on modulation of the intestine to regulate the alterations produced in obesity.  Final considerations:  It is shown the participation of the gut microbiota as a predisposing factor in the pathophysiology of obesity and its therapeutic modulation with various methods of biotherapy to reset the heterogeneity of the microbiome; among them are promising the use of prebiotics, probiotics, symbiotics and the transplantation of fecal microbiota.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[microbiota intestinal]]></kwd>
<kwd lng="es"><![CDATA[obesidad]]></kwd>
<kwd lng="es"><![CDATA[modulación microbiota intestinal]]></kwd>
<kwd lng="en"><![CDATA[gut microbiota]]></kwd>
<kwd lng="en"><![CDATA[obesity]]></kwd>
<kwd lng="en"><![CDATA[modulation intestinal microbiota]]></kwd>
</kwd-group>
</article-meta>
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