<?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%">Bernardi, Stella</style></author><author><style face="normal" font="default" size="100%">Fabris, Bruno</style></author><author><style face="normal" font="default" size="100%">Thomas, Merlin</style></author><author><style face="normal" font="default" size="100%">Toffoli, Barbara</style></author><author><style face="normal" font="default" size="100%">Tikellis, Christos</style></author><author><style face="normal" font="default" size="100%">Candido, Riccardo</style></author><author><style face="normal" font="default" size="100%">Catena, Cristiana</style></author><author><style face="normal" font="default" size="100%">Mulatero, Paolo</style></author><author><style face="normal" font="default" size="100%">Barbone, Fabio</style></author><author><style face="normal" font="default" size="100%">Radillo, Oriano</style></author><author><style face="normal" font="default" size="100%">Zauli, Giorgio</style></author><author><style face="normal" font="default" size="100%">Secchiero, Paola</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Osteoprotegerin increases in metabolic syndrome and promotes adipose tissue proinflammatory changes.</style></title><secondary-title><style face="normal" font="default" size="100%">Mol Cell Endocrinol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Mol. Cell. Endocrinol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adipose Tissue</style></keyword><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Blood Glucose</style></keyword><keyword><style  face="normal" font="default" size="100%">Body Mass Index</style></keyword><keyword><style  face="normal" font="default" size="100%">C-Reactive Protein</style></keyword><keyword><style  face="normal" font="default" size="100%">Case-Control Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Cholesterol, HDL</style></keyword><keyword><style  face="normal" font="default" size="100%">Cholesterol, LDL</style></keyword><keyword><style  face="normal" font="default" size="100%">Diet, High-Fat</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Inflammation</style></keyword><keyword><style  face="normal" font="default" size="100%">Insulin</style></keyword><keyword><style  face="normal" font="default" size="100%">Insulin Resistance</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Metabolic Syndrome X</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%">Middle Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Obesity</style></keyword><keyword><style  face="normal" font="default" size="100%">Osteoprotegerin</style></keyword><keyword><style  face="normal" font="default" size="100%">Triglycerides</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2014</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2014 Aug 25</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">394</style></volume><pages><style face="normal" font="default" size="100%">13-20</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;Inflammation is believed to link obesity to insulin resistance, as in the setting of metabolic syndrome (MetS). Osteoprotegerin (OPG) is a soluble protein that seems to exert proatherogenic and prodiabetogenic effects. This study aims at determining OPG levels in MetS and whether OPG might contribute to MetS development and progression.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODOLOGY/PRINCIPAL FINDINGS: &lt;/b&gt;Circulating OPG was measured in 46 patients with MetS and 63 controls, and was found significantly elevated in those with MetS. In addition, circulating and tissue OPG was significantly increased in high-fat diet (HFD) fed C57BL6 mice, which is one of the animal models for the study of MetS. To evaluate the consequences of OPG elevation, we delivered this protein to C57BL6 mice, finding that it promoted systemic and adipose tissue proinflammatory changes in association with metabolic abnormalities.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS/SIGNIFICANCE: &lt;/b&gt;These data suggest that OPG may trigger adipose tissue proinflammatory changes in MetS/HFD-induced obesity.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">1-2</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/24998520?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%">Bernardi, Stella</style></author><author><style face="normal" font="default" size="100%">Zauli, Giorgio</style></author><author><style face="normal" font="default" size="100%">Tikellis, Christos</style></author><author><style face="normal" font="default" size="100%">Candido, Riccardo</style></author><author><style face="normal" font="default" size="100%">Fabris, Bruno</style></author><author><style face="normal" font="default" size="100%">Secchiero, Paola</style></author><author><style face="normal" font="default" size="100%">Cooper, Mark E</style></author><author><style face="normal" font="default" size="100%">Thomas, Merlin C</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">TNF-related apoptosis-inducing ligand significantly attenuates metabolic abnormalities in high-fat-fed mice reducing adiposity and systemic inflammation.</style></title><secondary-title><style face="normal" font="default" size="100%">Clin Sci (Lond)</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Clin. Sci.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adiposity</style></keyword><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%">Calorimetry</style></keyword><keyword><style  face="normal" font="default" size="100%">Cytokines</style></keyword><keyword><style  face="normal" font="default" size="100%">Dietary Fats</style></keyword><keyword><style  face="normal" font="default" size="100%">Energy Intake</style></keyword><keyword><style  face="normal" font="default" size="100%">Glucose Tolerance Test</style></keyword><keyword><style  face="normal" font="default" size="100%">Hyperglycemia</style></keyword><keyword><style  face="normal" font="default" size="100%">Hyperinsulinism</style></keyword><keyword><style  face="normal" font="default" size="100%">Inflammation</style></keyword><keyword><style  face="normal" font="default" size="100%">Inflammation Mediators</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%">Oxidation-Reduction</style></keyword><keyword><style  face="normal" font="default" size="100%">Palmitic Acid</style></keyword><keyword><style  face="normal" font="default" size="100%">Real-Time Polymerase Chain Reaction</style></keyword><keyword><style  face="normal" font="default" size="100%">TNF-Related Apoptosis-Inducing Ligand</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2012 Nov</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">123</style></volume><pages><style face="normal" font="default" size="100%">547-55</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;TRAIL [TNF (tumour necrosis factor)-related apoptosis-inducing ligand] has recently been shown to ameliorate the natural history of DM (diabetes mellitus). It has not been determined yet whether systemic TRAIL delivery would prevent the metabolic abnormalities due to an HFD [HF (high-fat) diet]. For this purpose, 27 male C57bl6 mice aged 8 weeks were randomly fed on a standard diet, HFD or HFD+TRAIL for 12 weeks. TRAIL was delivered weekly by intraperitoneal injection. Body composition was evaluated; indirect calorimetry studies, GTT (glucose tolerance test) and ITT (insulin tolerance test) were performed. Pro-inflammatory cytokines, together with adipose tissue gene expression and apoptosis, were measured. TRAIL treatment reduced significantly the increased adiposity associated with an HFD. Moreover, it reduced significantly hyperglycaemia and hyperinsulinaemia during a GTT and it improved significantly the peripheral response to insulin. TRAIL reversed the changes in substrate utilization induced by the HFD and ameliorated skeletal muscle non-esterified fatty acids oxidation rate. This was associated with a significant reduction of pro-inflammatory cytokines together with a modulation of adipose tissue gene expression and apoptosis. These findings shed light on the possible anti-adipogenic and anti-inflammatory effects of TRAIL and open new therapeutic possibilities against obesity, systemic inflammation and T2DM (Type 2 DM).&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">9</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/22616837?dopt=Abstract</style></custom1></record></records></xml>