<?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%">Cobo-Vuilleumier, Nadia</style></author><author><style face="normal" font="default" size="100%">Lorenzo, Petra I</style></author><author><style face="normal" font="default" size="100%">Rodríguez, Noelia García</style></author><author><style face="normal" font="default" size="100%">Herrera Gómez, Irene de Gracia</style></author><author><style face="normal" font="default" size="100%">Fuente-Martin, Esther</style></author><author><style face="normal" font="default" size="100%">López-Noriega, Livia</style></author><author><style face="normal" font="default" size="100%">Mellado-Gil, José Manuel</style></author><author><style face="normal" font="default" size="100%">Romero-Zerbo, Silvana-Yanina</style></author><author><style face="normal" font="default" size="100%">Baquié, Mathurin</style></author><author><style face="normal" font="default" size="100%">Lachaud, Christian Claude</style></author><author><style face="normal" font="default" size="100%">Stifter, Katja</style></author><author><style face="normal" font="default" size="100%">Perdomo, German</style></author><author><style face="normal" font="default" size="100%">Bugliani, Marco</style></author><author><style face="normal" font="default" size="100%">De Tata, Vincenzo</style></author><author><style face="normal" font="default" size="100%">Bosco, Domenico</style></author><author><style face="normal" font="default" size="100%">Parnaud, Geraldine</style></author><author><style face="normal" font="default" size="100%">Pozo, David</style></author><author><style face="normal" font="default" size="100%">Hmadcha, Abdelkrim</style></author><author><style face="normal" font="default" size="100%">Florido, Javier P</style></author><author><style face="normal" font="default" size="100%">Toscano, Miguel G</style></author><author><style face="normal" font="default" size="100%">de Haan, Peter</style></author><author><style face="normal" font="default" size="100%">Schoonjans, Kristina</style></author><author><style face="normal" font="default" size="100%">Sánchez Palazón, Luis</style></author><author><style face="normal" font="default" size="100%">Marchetti, Piero</style></author><author><style face="normal" font="default" size="100%">Schirmbeck, Reinhold</style></author><author><style face="normal" font="default" size="100%">Martín-Montalvo, Alejandro</style></author><author><style face="normal" font="default" size="100%">Meda, Paolo</style></author><author><style face="normal" font="default" size="100%">Soria, Bernat</style></author><author><style face="normal" font="default" size="100%">Bermúdez-Silva, Francisco-Javier</style></author><author><style face="normal" font="default" size="100%">St-Onge, Luc</style></author><author><style face="normal" font="default" size="100%">Gauthier, Benoit R</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">LRH-1 agonism favours an immune-islet dialogue which protects against diabetes mellitus.</style></title><secondary-title><style face="normal" font="default" size="100%">Nat Commun</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Nat Commun</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Apoptosis</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Communication</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Survival</style></keyword><keyword><style  face="normal" font="default" size="100%">Diabetes Mellitus, Experimental</style></keyword><keyword><style  face="normal" font="default" size="100%">Diabetes Mellitus, Type 2</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%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Hypoglycemic Agents</style></keyword><keyword><style  face="normal" font="default" size="100%">Immunity, Innate</style></keyword><keyword><style  face="normal" font="default" size="100%">insulin</style></keyword><keyword><style  face="normal" font="default" size="100%">Insulin-Secreting Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Islets of Langerhans</style></keyword><keyword><style  face="normal" font="default" size="100%">Islets of Langerhans Transplantation</style></keyword><keyword><style  face="normal" font="default" size="100%">Macrophages</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice, Inbred C57BL</style></keyword><keyword><style  face="normal" font="default" size="100%">Phenalenes</style></keyword><keyword><style  face="normal" font="default" size="100%">Receptors, Cytoplasmic and Nuclear</style></keyword><keyword><style  face="normal" font="default" size="100%">Streptozocin</style></keyword><keyword><style  face="normal" font="default" size="100%">T-Lymphocytes, Regulatory</style></keyword><keyword><style  face="normal" font="default" size="100%">Transplantation, Heterologous</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2018</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2018 Apr 16</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">9</style></volume><pages><style face="normal" font="default" size="100%">1488</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Type 1 diabetes mellitus (T1DM) is due to the selective destruction of islet beta cells by immune cells. Current therapies focused on repressing the immune attack or stimulating beta cell regeneration still have limited clinical efficacy. Therefore, it is timely to identify innovative targets to dampen the immune process, while promoting beta cell survival and function. Liver receptor homologue-1 (LRH-1) is a nuclear receptor that represses inflammation in digestive organs, and protects pancreatic islets against apoptosis. Here, we show that BL001, a small LRH-1 agonist, impedes hyperglycemia progression and the immune-dependent inflammation of pancreas in murine models of T1DM, and beta cell apoptosis in islets of type 2 diabetic patients, while increasing beta cell mass and insulin secretion. Thus, we suggest that LRH-1 agonism favors a dialogue between immune and islet cells, which could be druggable to protect against diabetes mellitus.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">1</style></issue><custom1><style face="normal" font="default" size="100%">https://www.ncbi.nlm.nih.gov/pubmed/29662071?dopt=Abstract</style></custom1></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%">Sanghez, Valentina</style></author><author><style face="normal" font="default" size="100%">Cubuk, Cankut</style></author><author><style face="normal" font="default" size="100%">Sebastián-Leon, Patricia</style></author><author><style face="normal" font="default" size="100%">Carobbio, Stefania</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%">Bartolomucci, Alessandro</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Chronic subordination stress selectively downregulates the insulin signaling pathway in liver and skeletal muscle but not in adipose tissue of male mice.</style></title><secondary-title><style face="normal" font="default" size="100%">Stress (Amsterdam, Netherlands)</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adipose tissue</style></keyword><keyword><style  face="normal" font="default" size="100%">insulin</style></keyword><keyword><style  face="normal" font="default" size="100%">IRS1</style></keyword><keyword><style  face="normal" font="default" size="100%">IRS2</style></keyword><keyword><style  face="normal" font="default" size="100%">metabolic syndrome</style></keyword><keyword><style  face="normal" font="default" size="100%">obesity</style></keyword><keyword><style  face="normal" font="default" size="100%">pathway analysis</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2016</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2016 Mar 7</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.tandfonline.com/doi/abs/10.3109/10253890.2016.1151491?journalCode=ists20</style></url></web-urls></urls><pages><style face="normal" font="default" size="100%">1-11</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Chronic stress has been associated with obesity, glucose intolerance, and insulin resistance. We developed a model of chronic psychosocial stress (CPS) in which subordinate mice are vulnerable to obesity and the metabolic-like syndrome while dominant mice exhibit a healthy metabolic phenotype. Here we tested the hypothesis that the metabolic difference between subordinate and dominant mice is associated with changes in functional pathways relevant for insulin sensitivity, glucose and lipid homeostasis. Male mice were exposed to CPS for four weeks and fed either a standard diet or a high-fat diet (HFD). We first measured, by real-time PCR candidate genes, in the liver, skeletal muscle, and the perigonadal white adipose tissue (pWAT). Subsequently, we used a probabilistic analysis approach to analyze different ways in which signals can be transmitted across the pathways in each tissue. Results showed that subordinate mice displayed a drastic downregulation of the insulin pathway in liver and muscle, indicative of insulin resistance, already on standard diet. Conversely, pWAT showed molecular changes suggestive of facilitated fat deposition in an otherwise insulin-sensitive tissue. The molecular changes in subordinate mice fed a standard diet were greater compared to HFD-fed controls. Finally, dominant mice maintained a substantially normal metabolic and molecular phenotype even when fed a HFD. Overall, our data demonstrate that subordination stress is a potent stimulus for the downregulation of the insulin signaling pathway in liver and muscle and a major risk factor for the development of obesity, insulin resistance, and type 2 diabetes mellitus.</style></abstract></record></records></xml>