109 research outputs found
Peroxisome Proliferator-Activated Receptors (PPARs) in Glucose Control
No full textThe peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors that control lipid and glucose metabolism. PPARs regulate gene expression by binding with retinoid X receptor as a heterodimeric partner to specific DNA sequences, termed PPAR response elements. In addition, PPARs may modulate gene transcription by directly interfering with other transcription factor pathways in a DNA-binding independent manner. To date, three different PPAR isoforms, designated α, β/δ, and γ, have been identified. PPAR-γ was the first isoform demonstrated to affect carbohydrate metabolism and PPAR-γ agonists, the thiazolidinediones, are now in clinical use for the treatment of insulin resistance. Unexpectedly, later studies revealed that also the other two isoforms modulate glucose metabolism. Here we summarize our understanding on how these nuclear receptor isoforms are involved in the control of glucose metabolism, describing some of the novel regulatory mechanisms. In addition, this chapter reviews the evidence and recent developments relating to the role of some foods containing natural compounds as PPAR agonists
INTEGRAZIONE E VALORIZZAZIONE DEL RUDERE ARCHEOLOGICO NEI CONTESTI URBANI STORICIZZATI
No full textL'archeologia urbana è una fonte importante di informazioni per conoscere la storia e la cultura di una città. Promuovere la conoscenza, la conservazione e la valorizzazione dei siti urbani storici e archeologici è fondamentale per ricostruire la dimensione diacronica e diatopica del passato, attraverso l'uso di strumenti cognitivi e delle competenze tecniche. E’ fondamentale conferire ai resti del passato nuovi significati e adeguate complessità sia di tipo urbanistico-funzionale, che di tipo architettonico-simbolico. L’archeologia dovrebbe proporsi come uno strumento concreto di costruzione della memoria culturale
Editorial: Nutritional modulation of central nervous system development, maintenance, plasticity, and recovery
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A Selective IκB Kinase Inhibitor (IKK16) Attenuates The Organ Injury / Dysfunction Associated With Haemorrhagic Shock In The Rat
No full textA short bout of HFD promotes long-lasting hepatic lipid accumulation
No full textA short bout of high fat diet (HFD) impairs glucose tolerance and induces hepatic steatosis in mice. Here, we aimed to elaborate on long-lasting effects of short-term high fat feeding. As expected, one week of HFD significantly impaired glucose tolerance. Intriguingly, recovery feeding with a standard rodent diet for 8 weeks did not fully normalize glucose tolerance. In addition, mice exposed to a short bout of HFD revealed significantly increased liver fat accumulation paralleled by elevated portal free fatty acid levels after 8 weeks of recovery feeding compared to exclusively chow-fed littermates. In conclusion, a short bout of HFD has long-lasting effects on hepatic lipid accumulation and glucose tolerance
Endogenous annexin-A1 is a protective determinant in high-fat diet (HFD)-induced insulin resistance and diabetic nephropathy
No full textEndogenous Annexin-A1 is a Protective Determinant in HFD-induced Insulin Resistance and Diabetic Nephropathy
No full textThe NLRP3 Inflammasome as a Novel Player of the Intercellular Crosstalk in Metabolic Disorders
No full textThe combination of obesity and type 2 diabetes is a serious health problem, which is projected to afflict 300 million people worldwide by 2020. Both clinical and translational laboratory studies have demonstrated that chronic inflammation is associated with obesity and obesity-related conditions such as insulin resistance. However, the precise etiopathogenetic mechanisms linking obesity to diabetes remain to be elucidated, and the pathways that mediate this phenomenon are not fully characterized. One of the most recently identified signaling pathways, whose activation seems to affect many metabolic disorders, is the “inflammasome,” a multiprotein complex composed of NLRP3 (nucleotide-binding domain and leucine-rich repeat protein 3), ASC (apoptosis-associated speck-like protein containing a CARD), and procaspase-1. NLRP3 inflammasome activation leads to the processing and secretion of the proinflammatory cytokines interleukin- (IL-) 1β and IL-18. The goal of this paper is to review new insights on the effects of the NLRP3 inflammasome activation in the complex mechanisms of crosstalk between different organs, for a better understanding of the role of chronic inflammation in metabolic disease pathogenesis. We will provide here a perspective on the current research on NLRP3 inflammasome, which may represent an innovative therapeutic target to reverse the detrimental metabolic consequences of the metabolic inflammation
Gender Dimorphism of the Cardiac Dysfunction in Murine Sepsis: Signalling Mechanisms and Age-Dependency
No full textThis is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.JC is supported by a jointly funded PhD-studentship of the China Scholarship Council (grant number 201206240146) and Queen Mary University of London (QMUL). SMC is supported by a Research Fellowship of the German Research Foundation (Deutsche Forschungsgemeinschaft; DFG CO 912/1-1). NSAP is, in part, supported by the Bart’s and The London Charity (753/1722). This work is supported, in part, by the William Harvey Research Foundation and by a grant from the University of Turin (Ricerca Locale ex-60% 2013). This work forms part of the research themes contributing to the translational research portfolio of Barts and the London Cardiovascular Biomedical Research Unit, which is supported and funded by the National Institute of Health Research. This work also contributes to the Organ Protection research theme of the Barts Centre for Trauma Sciences, supported by the Barts and The London Charity (Award 753/1722)
Artesunate protects against the organ injury and dysfunction induced by severe hemorrhage and resuscitation
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