85 research outputs found

    Social stress, obesity and glucose tolerance: a psychobiological investigation

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    Social stress, obesity and glucose tolerance: a psychobiological investigation Stress has been associated with changes in eating behavior and food preferences (Dallman et al. 2003). In humans psychosocial and socio-economical challenges have been related with neuroendocrine-autonomic dysregulation followed by visceral obesity and increased in body mass index (BMI) (Van Strien et al. 1986, Rosmond, Dallman and Björntorp 1998). The chronic activation of stress response system, leads to an increase in food intake, especially high palatable food (Dallman et al. 2004, Dallman et al. 2005), obesity and metabolic syndrome (Rosmond et al. 1998, Björntorp 1993, Björntorp 1996a, Tsigos and Chrousos 2002). Altogether these metabolic disorders result in a pre-diabetic state, which may turn in type 2 diabetes (T2D) in susceptible individuals in a nutrional rich environment (Björntorp 1996b, Boden 2002, Chan et al. 1994, Colditz et al. 1990, DeFronzo 2004). In addition, comorbid pathology such as “atypical depression” linked to stress (DSM-IV, American Psychiatric Association, 2000) has been associated to eating disorders-induced obesity.(Mitchell and Mussell 1995, Stein et al. 2007, Stunkard 2011). While several genetic or pharmacological animal models of metabolic syndrome and T2D have been developed, so far there is a paucity of models in which the diseases are triggered by psychogenic stimuli. Aim of the present study is: Chapter One: the original characterization of a mouse models of early metabolic syndrome/T2D onset induced by exposing mice to chronic subordination stress in the presence of high fat diet. Chapter Two: determine if vulnerability to stress induced metabolic disease is status dependent. Specifically we will directly compare the metabolic consequences of being high in rank (dominant) and low in rank (subordinate) in mice exposed to our model of chronic psychosocial stress CPS and HFD Chapter Three: characterized if CPS may be considered a model of stress- induced binge eating disorders (BED) and understand the role of hyperphagia in stressed-induced obesity and T2D using a Pair-feeding protocol

    Valorizzazione di clean biogas mediante reazione di reforming

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    Sono stati studiati catalizzatori a base di Ni e Ni-Rh supportati su Mg/Al/O, ottenuti per co-precipitazione di precursori tipo idrotalcite, nelle reazioni di Dry Reforming (DR) e Steam/Dry Reforming (S/DR) di clean biogas, modificando la formulazione del catalizzatore per migliorarne le prestazioni. La temperatura promuoveva l’attività catalitica e riduceva la formazione di coke. Il Rh formava una lega con il Ni riducendo le dimensioni della fase attiva e la formazione di coke, anche se buone prestazioni si ottenevano solo ad elevata temperatura. Nello S/DR era possibile modulare la quantità di vapore usata ottenendo rapporti H2/CO idonei per l’uso nella sintesi di metanolo o idrocarburi; in queste condizioni i catalizzatori Ni-Rh mostravano una bassa produzione di coke. Infine variando la quantità di Mg nel catalizzatore si variavano le proprietà acido-base del supporto e la sua interazione con la fase attiva, modificando l’attività e la stabilità del catalizzatore. They have been studied Ni and Ni-Rh based catalysts supported on Mg/Al/O, prepared by co-precipitation of hydrotalcite-type precursors, for Dry Reforming (DR) and Steam/Dry Reforming (S/DR) reaction of clean biogas, modifying the formulation to increase the performance. Temperature promoted the catalytic activity and reduced the coke formation. Rh formed an alloy with Ni, decreasing the size of the active phase and the coke formation, although good performance were achieved only at high temperature. In S/DR it was also possible to modify the amount of steam used obtaining H2/CO ratios suitable for the methanol or hydrocarbon synthesis, under these conditions the Ni-Rh catalysts showed a low production of coke. Finally, varying the amount of Mg in the catalyst, it changed the acid-base properties of the support and its interaction with the active phase, determining the activity and stability of the catalyst

    Notch activation is required for downregulation of HoxA3-dependent endothelial cell phenotype during blood formation.

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    Hemogenic endothelium (HE) undergoes endothelial-to-hematopoietic transition (EHT) to generate blood, a process that requires progressive down-regulation of endothelial genes and induction of hematopoietic ones. Previously, we have shown that the transcription factor HoxA3 prevents blood formation by inhibiting Runx1 expression, maintaining endothelial gene expression and thus blocking EHT. In the present study, we show that HoxA3 also prevents blood formation by inhibiting Notch pathway. HoxA3 induced upregulation of Jag1 ligand in endothelial cells, which led to cis-inhibition of the Notch pathway, rendering the HE nonresponsive to Notch signals. While Notch activation alone was insufficient to promote blood formation in the presence of HoxA3, activation of Notch or downregulation of Jag1 resulted in a loss of the endothelial phenotype which is a prerequisite for EHT. Taken together, these results demonstrate that Notch pathway activation is necessary to downregulate endothelial markers during EHT

    Chronic subordination stress selectively downregulates the insulin signaling pathway in liver and skeletal muscle but not in adipose tissue of male mice

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    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.Supported by UofMN Medical School start-up funds to AB, Medical Research Council MRC Disease Model Core and British Heart Foundation program grants to AVP, and BIO2011-27069 from the Spanish Ministry of Economy and Competitiveness and PROMETEOII/2014/025 from the GVA-FEDER to JD. VS was supported by a graduate student fellowship of the University of Parma. CC was supported by EU FP7-People Project(ref 316861) "MLPM2012: Machine Learning For Personalized Medicine".This is the final version of the article. It first appeared from Taylor & Francis via http://dx.doi.org/10.3109/10253890.2016.115149

    Chronic subordination stress selectively downregulates the insulin signaling pathway in liver and skeletal muscle but not in adipose tissue of male mice.

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    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.Supported by UofMN Medical School start-up funds to AB, Medical Research Council MRC Disease Model Core and British Heart Foundation program grants to AVP, and BIO2011-27069 from the Spanish Ministry of Economy and Competitiveness and PROMETEOII/2014/025 from the GVA-FEDER to JD. VS was supported by a graduate student fellowship of the University of Parma. CC was supported by EU FP7-People Project(ref 316861) "MLPM2012: Machine Learning For Personalized Medicine".This is the final version of the article. It first appeared from Taylor & Francis via http://dx.doi.org/10.3109/10253890.2016.115149

    Ru–CeO2 and Ni–CeO2 Coated on Open-Cell Metallic Foams by Electrodeposition for the CO2 Methanation

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    CO2 methanation structured catalysts, made by a layer of Ru–CeO2 or Ni–CeO2 (Ru/Ce = 3/97; Ni/Ce = 1/3 and 3/1) on open-cell NiCrAl foams, are prepared by electrodeposition and a subsequent calcination step. The performance of the catalysts at a space velocity of 320,000 mL gcat–1 h–1 in a feedstock with H2/CO2/N2 = 4/1/1 v/v, significantly depends on the Ni content and the preparation method. A low Ru or Ni content promotes the metal–CeO2 interaction, the formation of defects in CeO2 as well as the development of a lower amount of cracks in the coating; however, the catalysts show a poor CO2 conversion and selectivity to CH4. The CH4 production rate at low temperature largely increases for the high Ni loaded catalyst, 68.7 LCH4 gNi–1 h–1 at 350 °C oven temperature. This productivity is similar to the value obtained with a Ni3Ce1 pellet catalyst prepared by the coprecipitation method, a behavior not achievable for low Ru- and Ni-loaded catalysts

    An efficient and reproducible method for transformation of genetically recalcitrant bifidobacteria

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    This study describes an efficient transformation system for the introduction of plasmid DNA into Bifidobacterium bifidum PRL2010 and Bifidobacterium asteroides PRL2011, for which to the best of our knowledge no transformation data have been reported previously. The method is based on electroporation of bifidobacterial cells, which were made competent by an optimized methodology based on varying media and growth conditions. Furthermore, the transformation protocol was applied in order to design a PRL2010-derivative, which carries antibiotic resistance against chloramphenicol and which was used to monitor PRL2010 colonization in a murine model

    AgCu Bimetallic Electrocatalysts for the Reduction of Biomass-Derived Compounds

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    The electrochemical transformation of biomass-derived compounds (e.g., aldehyde electroreduction to alcohols) is gaining increasing interest due to the sustainability of this process that can be exploited to produce value-added products from biowastes and renewable electricity. In this framework, the electrochemical conversion of 5-hydroxymethylfurfural (HMF) to 2,5-bis(hydroxymethyl)furan (BHMF) is studied. Nanostructured Ag deposited on Cu is an active and selective electrocatalyst for the formation of BHMF in basic media. However, this catalyst deserves further research to elucidate the role of the morphology and size of the coated particles in its performance as well as the actual catalyst surface composition and its stability. Herein, Ag is coated on Cu open-cell foams by electrodeposition and galvanic displacement to generate different catalyst morphologies, deepening on the particle growth mechanism, and the samples are compared with bare Ag and Cu foams. The chemical–physical and electrochemical properties of the as-prepared and spent catalysts are correlated to the electroactivity in the HMF conversion and its selectivity toward the formation of BHMF during electroreduction. AgCu bimetallic nanoparticles or dendrites are formed on electrodeposited and displaced catalysts, respectively, whose surface is Cu-enriched along with electrochemical tests. Both types of bimetallic AgCu particles evidence a superior electroactive surface area as well as an enhanced charge and mass transfer in comparison with the bare Ag and Cu foams. These features together with a synergistic role between Ag and Cu superficial active sites could be related to the twofold enhanced selectivity of the Ag/Cu catalysts for the selective conversion of HMF to BHMF, that is, >80% selectivity and ∼ 100% conversion, and BHMF productivity values (0.206 and 0.280 mmol cm–2 h–1) ca. 1.5–3 times higher than those previously reported
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