<?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>2007-1523</journal-id>
<journal-title><![CDATA[Revista mexicana de trastornos alimentarios]]></journal-title>
<abbrev-journal-title><![CDATA[Rev. Mex. de trastor. aliment]]></abbrev-journal-title>
<issn>2007-1523</issn>
<publisher>
<publisher-name><![CDATA[Universidad Nacional Autónoma de México, Facultad de Estudios Superiores Iztacala]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S2007-15232023000200170</article-id>
<article-id pub-id-type="doi">10.22201/fesi.20071523e.2023.2.754</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[La alteración hipotalámica en la obesidad: neuroinflamación y disfunción metabólica]]></article-title>
<article-title xml:lang="en"><![CDATA[The hypotalamic disturbances during obesity: neuroinflammation and metabolic dysfunction]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Torres Guerrero]]></surname>
<given-names><![CDATA[Haydee]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Ramírez Carreto]]></surname>
<given-names><![CDATA[Ricardo Jair]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Rodríguez Cortés]]></surname>
<given-names><![CDATA[Yesica María]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Chavarría]]></surname>
<given-names><![CDATA[Anahí]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Universidad Nacional Autónoma de México Facultad de Medicina Unidad de Investigación en Medicina Experimental]]></institution>
<addr-line><![CDATA[ Ciudad de México]]></addr-line>
<country>Mexico</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>12</month>
<year>2023</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>12</month>
<year>2023</year>
</pub-date>
<volume>13</volume>
<numero>2</numero>
<fpage>170</fpage>
<lpage>186</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_arttext&amp;pid=S2007-15232023000200170&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_abstract&amp;pid=S2007-15232023000200170&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_pdf&amp;pid=S2007-15232023000200170&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen La obesidad es considerada actualmente como un problema de salud pública global y se caracteriza por la hipertrofia e hiperplasia del tejido adiposo debido a la ingesta hipercalórica y la falta de actividad física, disfunción metabólica, inflamación sistémica crónica de bajo grado y gradualmente neuroinflamación hipotalámica. El tejido adiposo actúa como un órgano endocrino secretando adipocinas y citocinas que actúan como reguladores del metabolismo. Sin embargo, la presencia de niveles elevados de ácidos grasos libres y de moléculas inflamatorias derivadas de los adipocitos, pueden alterar la respuesta inmunitaria sistémica, generando inflamación crónica, comprometiendo la integridad de la barrera hematoencefálica y estimulando la respuesta de la glía, especialmente en regiones específicas del hipotálamo, centro de regulación de la homeostasis energética. Las células gliales hipotalámicas son importantes en la transmisión de señales inflamatorias relacionadas con la dieta, pueden modular la actividad neuronal, responder a las señales inmunológicas periféricas e iniciar una respuesta inflamatoria local y gliosis. Esta revisión se enfoca en la descripción general de la disfunción metabólica asociada a la obesidad y su participación en la alteración de la regulación hipotalámica, provocando neuroinflamación y modificaciones en la conducta alimentaria.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract  Nowadays, obesity is considered a worldwide rising health problem and is characterized by adipose tissue hypertrophy and hyperplasia due to hypercaloric intake and lack of physical activity, promoting the development of metabolic dysfunction, low-grade systemic chronic inflammation, and gradually hypothalamic neuroinflammation. Adipose tissue acts as an endocrine organ secreting adipokines and cytokines around peripheral organs, functioning as a master metabolism regulator. However, high levels of adipocyte-derived free fatty acids and inflammatory molecules promote impairments in systemic immune response, generate chronic inflammation, disrupt the blood-brain barrier, and stimulate glia, specifically in some hypothalamic regions, the master regulators of energetic homeostasis. Hypothalamic glial cells are essential in diet-related inflammatory signals transmission and can modulate neuronal activity, also respond to peripheral inflammatory signals and begin local inflammatory response and gliosis. This review aims to analyze obesity-related metabolic dysfunction and how it participates in the hypothalamic regulation impairments due to neuroinflammation and impairment in food intake behavior.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[Neuroinflamación]]></kwd>
<kwd lng="es"><![CDATA[hipotálamo]]></kwd>
<kwd lng="es"><![CDATA[obesidad]]></kwd>
<kwd lng="es"><![CDATA[microglía]]></kwd>
<kwd lng="es"><![CDATA[astrocitos]]></kwd>
<kwd lng="en"><![CDATA[Neuroinflammation]]></kwd>
<kwd lng="en"><![CDATA[hypothalamus]]></kwd>
<kwd lng="en"><![CDATA[obesity]]></kwd>
<kwd lng="en"><![CDATA[microglia]]></kwd>
<kwd lng="en"><![CDATA[astrocytes]]></kwd>
</kwd-group>
</article-meta>
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