<?xml version="1.0" encoding="UTF-8"?><?xml-stylesheet type="text/xsl" href="static/style.xsl"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-06-29T22:13:33Z</responseDate><request verb="GetRecord" identifier="oai:riubu.ubu.es:10259/9924" metadataPrefix="edm">https://riubu.ubu.es/oai/request</request><GetRecord><record><header><identifier>oai:riubu.ubu.es:10259/9924</identifier><datestamp>2025-01-16T01:05:34Z</datestamp><setSpec>com_10259_4862</setSpec><setSpec>com_10259_5086</setSpec><setSpec>com_10259_2604</setSpec><setSpec>col_10259_4863</setSpec></header><metadata><rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:doc="http://www.lyncode.com/xoai" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:ore="http://www.openarchives.org/ore/terms/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:ds="http://dspace.org/ds/elements/1.1/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:edm="http://www.europeana.eu/schemas/edm/" xsi:schemaLocation="http://www.w3.org/1999/02/22-rdf-syntax-ns# http://www.europeana.eu/schemas/edm/EDM.xsd">
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<dc:creator>Herrerías-González, Fernando</dc:creator>
<dc:creator>Yeramian, Andrée</dc:creator>
<dc:creator>Baena-Fustegueras, Juan Antonio</dc:creator>
<dc:creator>Bueno, Marta</dc:creator>
<dc:creator>Fleitas, Catherine</dc:creator>
<dc:creator>de la Fuente, Maricruz</dc:creator>
<dc:creator>Serrano, José C. E.</dc:creator>
<dc:creator>Granado-Serrano, Ana</dc:creator>
<dc:creator>Santamaría, Maite</dc:creator>
<dc:creator>Yeramian Hakim, Nadine</dc:creator>
<dc:creator>Zorzano-Martínez, Marta</dc:creator>
<dc:creator>Mora, Conchi</dc:creator>
<dc:creator>Lecube, Albert</dc:creator>
<dc:date>2023-05</dc:date>
<dc:description>Adipocyte dysfunction is the driver of obesity and correlates with insulin resistance and the&#xd;
onset of type 2 diabetes. Protein kinase N1 (PKN1) is a serine/threonine kinase that has been shown&#xd;
to contribute to Glut4 translocation to the membrane and glucose transport. Here, we evaluated the&#xd;
role of PKN1 in glucose metabolism under insulin-resistant conditions in primary visceral adipose&#xd;
tissue (VAT) from 31 patients with obesity and in murine 3T3-L1 adipocytes. In addition, in vitro&#xd;
studies in human VAT samples and mouse adipocytes were conducted to investigate the role of&#xd;
PKN1 in the adipogenic maturation process and glucose homeostasis control. We show that insulinresistant adipocytes present a decrease in PKN1 activation levels compared to nondiabetic control&#xd;
counterparts. We further show that PKN1 controls the adipogenesis process and glucose metabolism.&#xd;
PKN1-silenced adipocytes present a decrease in both differentiation process and glucose uptake,&#xd;
with a concomitant decrease in the expression levels of adipogenic markers, such as PPARγ, FABP4,&#xd;
adiponectin and CEBPα. Altogether, these results point to PKN1 as a regulator of key signaling&#xd;
pathways involved in adipocyte differentiation and as an emerging player of adipocyte insulin&#xd;
responsiveness. These findings may provide new therapeutic approaches for the management of&#xd;
insulin resistance in type 2 diabetes.</dc:description>
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<dc:identifier>http://hdl.handle.net/10259/9924</dc:identifier>
<dc:language>spa</dc:language>
<dc:publisher>MDPI</dc:publisher>
<dc:title>PKN1 Kinase: A Key Player in Adipocyte Differentiation and Glucose Metabolism</dc:title>
<dc:type>info:eu-repo/semantics/article</dc:type>
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