<?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>0121-0807</journal-id>
<journal-title><![CDATA[Revista de la Universidad Industrial de Santander. Salud]]></journal-title>
<abbrev-journal-title><![CDATA[Rev. Univ. Ind. Santander. Salud]]></abbrev-journal-title>
<issn>0121-0807</issn>
<publisher>
<publisher-name><![CDATA[Universidad Industrial de Santander]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S0121-08072022000100335</article-id>
<article-id pub-id-type="doi">10.18273/saluduis.54.e:22012</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Hipertrofia y resistencia a la insulina en un modelo in vitro de obesidad y DMT2 inducida por alta glucosa e insulina]]></article-title>
<article-title xml:lang="en"><![CDATA[Hypertrophy and insulin resistance in an in vitro model of obesity and T2DM induced by high glucose and insulin]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Bonilla-Carvajal]]></surname>
<given-names><![CDATA[Katherin]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Ángel-Martín]]></surname>
<given-names><![CDATA[Alberto]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Moreno-Castellanos]]></surname>
<given-names><![CDATA[Natalia]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Universidad Industrial de Santander  ]]></institution>
<addr-line><![CDATA[Bucaramanga ]]></addr-line>
<country>Colombia</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>12</month>
<year>2022</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>12</month>
<year>2022</year>
</pub-date>
<volume>54</volume>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.co/scielo.php?script=sci_arttext&amp;pid=S0121-08072022000100335&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.co/scielo.php?script=sci_abstract&amp;pid=S0121-08072022000100335&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.co/scielo.php?script=sci_pdf&amp;pid=S0121-08072022000100335&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen  Introducción: La obesidad es considerada un factor de riesgo para desarrollar resistencia a la insulina. La expansión del tejido adiposo se ha relacionado con el aumento de la producción de citoquinas proinflamatorias que, junto a los ácidos grasos son responsables, al menos en parte, del desarrollo de la resistencia a la insulina y esta a su vez, facilita el desarrollo de diabetes mellitus tipo 2 (DMT2).  Objetivo: El propósito de este estudio fue realizar y caracterizar un modelo in vitro de obesidad empleando concentraciones altas de glucosa e insulina en una línea de células adipocitarias.  Métodos: Se indujo modelo de hipertrofia celular realizando un estímulo en adipocitos maduros con una concentración de glucosa (450 mg/dL) e insulina (106 pmol/L) (modelo HGHI). Tras estímulo se realizaron ensayos de viabilidad celular, diámetro celular, movilización de lípidos y marcadores de señalización de insulina.  Resultados: Tras el tratamiento con HGHI, se evidencia hipertrofia adipocitaria, incremento en la acumulación de lípidos, reducción de la ruptura de éstos, alteración de la señalización de insulina y tendencia a modificación de proteínas de marcadores de estrés de retículo y estrés oxidativo.  Conclusión: Estos resultados demuestran la validez del modelo in vitro que simula al menos en parte la obesidad asociada a insulino resistencia, siendo una herramienta útil para estudiar los mecanismos de susceptibilidad a obesidad y resistencia a la insulina inducida in vitro con diferentes moléculas.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract  Introduction: Obesity is considered a risk factor for developing insulin resistance. The increase in adipose tissue has been related to the increase in the production of pro-inflammatory cytokines, which together with fatty acids are responsible, at least in part, for the development of insulin resistance, and this in turn facilitates the development of T2 diabetes mellitus type 2 (DMT2).  Objective: The purpose of this study was to perform and characterize an in vitro model of obesity using high concentrations of glucose and insulin on an adipocyte cell line.  Methods: A cell hypertrophy model was induced by stimulating mature adipocytes with a concentration of glucose (450 mg/dL) and insulin (106 pmol/L) (HGHI model). The cell viability, cell diameter, lipid mobilization and insulin signalling markers were evaluated.  Results: After HGHI treatment, adipocytes show hypertrophy, increase in lipid accumulation, reduction of lipid breakdown, alteration of insulin signalling, a tendency to modify proteins of reticulum stress markers and, oxidative stress.  Conclusion: These results demonstrate a new in vitro model that simulates, at least in part, obesity associated with insulin resistance being a useful tool to study the mechanisms of susceptibility to obesity and insulin resistance induced in vitro by different molecules.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[Adipocitos]]></kwd>
<kwd lng="es"><![CDATA[Lipogénesis]]></kwd>
<kwd lng="es"><![CDATA[Lipólisis]]></kwd>
<kwd lng="es"><![CDATA[Glucosa]]></kwd>
<kwd lng="es"><![CDATA[Insulina]]></kwd>
<kwd lng="en"><![CDATA[Adipocytes]]></kwd>
<kwd lng="en"><![CDATA[Lipogenesis]]></kwd>
<kwd lng="en"><![CDATA[Lipolysis]]></kwd>
<kwd lng="en"><![CDATA[Glucose]]></kwd>
<kwd lng="en"><![CDATA[Insulin]]></kwd>
</kwd-group>
</article-meta>
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