<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Pellegrinelli, Vanessa</style></author><author><style face="normal" font="default" size="100%">Figueroa-Juárez, Elizabeth</style></author><author><style face="normal" font="default" size="100%">Samuelson, Isabella</style></author><author><style face="normal" font="default" size="100%">U-Din, Mueez</style></author><author><style face="normal" font="default" size="100%">Rodriguez-Fdez, Sonia</style></author><author><style face="normal" font="default" size="100%">Virtue, Samuel</style></author><author><style face="normal" font="default" size="100%">Leggat, Jennifer</style></author><author><style face="normal" font="default" size="100%">Cubuk, Cankut</style></author><author><style face="normal" font="default" size="100%">Peirce, Vivian J</style></author><author><style face="normal" font="default" size="100%">Niemi, Tarja</style></author><author><style face="normal" font="default" size="100%">Campbell, Mark</style></author><author><style face="normal" font="default" size="100%">Rodriguez-Cuenca, Sergio</style></author><author><style face="normal" font="default" size="100%">Dopazo, Joaquin</style></author><author><style face="normal" font="default" size="100%">Carobbio, Stefania</style></author><author><style face="normal" font="default" size="100%">Virtanen, Kirsi A</style></author><author><style face="normal" font="default" size="100%">Vidal-Puig, Antonio</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Defective extracellular matrix remodeling in brown adipose tissue is associated with fibro-inflammation and reduced diet-induced thermogenesis.</style></title><secondary-title><style face="normal" font="default" size="100%">Cell Rep</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Cell Rep</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2023</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2023 Jun 13</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">42</style></volume><pages><style face="normal" font="default" size="100%">112640</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;The relevance of extracellular matrix (ECM) remodeling is reported in white adipose tissue (AT) and obesity-related dysfunctions, but little is known about the importance of ECM remodeling in brown AT (BAT) function. Here, we show that a time course of high-fat diet (HFD) feeding progressively impairs diet-induced thermogenesis concomitantly with the development of fibro-inflammation in BAT. Higher markers of fibro-inflammation are associated with lower cold-induced BAT activity in humans. Similarly, when mice are housed at thermoneutrality, inactivated BAT features fibro-inflammation. We validate the pathophysiological relevance of BAT ECM remodeling in response to temperature challenges and HFD using a model of a primary defect in the collagen turnover mediated by partial ablation of the Pepd prolidase. Pepd-heterozygous mice display exacerbated dysfunction and BAT fibro-inflammation at thermoneutrality and in HFD. Our findings show the relevance of ECM remodeling in BAT activation and provide a mechanism for BAT dysfunction in obesity.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">6</style></issue></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Vivas, Yurena</style></author><author><style face="normal" font="default" size="100%">Martinez-Garcia, Cristina</style></author><author><style face="normal" font="default" size="100%">Izquierdo, Adriana</style></author><author><style face="normal" font="default" size="100%">Garcia-Garcia, Francisco</style></author><author><style face="normal" font="default" size="100%">Callejas, Sergio</style></author><author><style face="normal" font="default" size="100%">Velasco, Ismael</style></author><author><style face="normal" font="default" size="100%">Campbell, Mark</style></author><author><style face="normal" font="default" size="100%">Ros, Manuel</style></author><author><style face="normal" font="default" size="100%">Dopazo, Ana</style></author><author><style face="normal" font="default" size="100%">Dopazo, Joaquin</style></author><author><style face="normal" font="default" size="100%">Vidal-Puig, Antonio</style></author><author><style face="normal" font="default" size="100%">Medina-Gomez, Gema</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Early peroxisome proliferator-activated receptor gamma regulated genes involved in expansion of pancreatic beta cell mass.</style></title><secondary-title><style face="normal" font="default" size="100%">BMC Med Genomics</style></secondary-title><alt-title><style face="normal" font="default" size="100%">BMC Med Genomics</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Proliferation</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Survival</style></keyword><keyword><style  face="normal" font="default" size="100%">Cholesterol</style></keyword><keyword><style  face="normal" font="default" size="100%">Down-Regulation</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression Regulation</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Knockout Techniques</style></keyword><keyword><style  face="normal" font="default" size="100%">Insulin Resistance</style></keyword><keyword><style  face="normal" font="default" size="100%">Insulin-Secreting Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice</style></keyword><keyword><style  face="normal" font="default" size="100%">obesity</style></keyword><keyword><style  face="normal" font="default" size="100%">Oxidation-Reduction</style></keyword><keyword><style  face="normal" font="default" size="100%">Phosphorylation</style></keyword><keyword><style  face="normal" font="default" size="100%">PPAR gamma</style></keyword><keyword><style  face="normal" font="default" size="100%">Signal Transduction</style></keyword><keyword><style  face="normal" font="default" size="100%">Transcription, Genetic</style></keyword><keyword><style  face="normal" font="default" size="100%">Transforming Growth Factor beta</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2011</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2011 Dec 30</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">4</style></volume><pages><style face="normal" font="default" size="100%">86</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;BACKGROUND: &lt;/b&gt;The progression towards type 2 diabetes depends on the allostatic response of pancreatic beta cells to synthesise and secrete enough insulin to compensate for insulin resistance. The endocrine pancreas is a plastic tissue able to expand or regress in response to the requirements imposed by physiological and pathophysiological states associated to insulin resistance such as pregnancy, obesity or ageing, but the mechanisms mediating beta cell mass expansion in these scenarios are not well defined. We have recently shown that ob/ob mice with genetic ablation of PPARγ2, a mouse model known as the POKO mouse failed to expand its beta cell mass. This phenotype contrasted with the appropriate expansion of the beta cell mass observed in their obese littermate ob/ob mice. Thus, comparison of these models islets particularly at early ages could provide some new insights on early PPARγ dependent transcriptional responses involved in the process of beta cell mass expansion&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Here we have investigated PPARγ dependent transcriptional responses occurring during the early stages of beta cell adaptation to insulin resistance in wild type, ob/ob, PPARγ2 KO and POKO mice. We have identified genes known to regulate both the rate of proliferation and the survival signals of beta cells. Moreover we have also identified new pathways induced in ob/ob islets that remained unchanged in POKO islets, suggesting an important role for PPARγ in maintenance/activation of mechanisms essential for the continued function of the beta cell.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;Our data suggest that the expansion of beta cell mass observed in ob/ob islets is associated with the activation of an immune response that fails to occur in POKO islets. We have also indentified other PPARγ dependent differentially regulated pathways including cholesterol biosynthesis, apoptosis through TGF-β signaling and decreased oxidative phosphorylation.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">https://www.ncbi.nlm.nih.gov/pubmed/22208362?dopt=Abstract</style></custom1></record></records></xml>