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Obesity prevalence is increasing in industrialized countries; it is considered as a major problem of public health, because it favours the appearance of dyslipidemia, steatosis, hypertension and insulin resistance . Abnormal accumulation of fat leads to the secretion of fatty acids and adipokines by adipocytes, which are implicated in the development of insulin resistance and other metabolic disturbances. A better comprehension of other molecular and cellular targets involved in obesity will help to understand how new therapeutic/nutritional approaches could be useful to counteract the progression of obesity-associated diseases.In this context two in vivo studies have been performed to analyze: -the involvement of the nuclear receptor PPAR-a. in the effects of oligofructose (OFS), a non digestible fibre fermented in the caeco-colon. PPAR-a. is widely implicated in food intake, lipid metabolism and glucose response. OFS has already shown numerous beneficial effects in various obesity models in rodents.-the contribution of Kupffer cells in the development of obesity and associated disorders. These hepatic macrophages seem to be implicated in hepatic deteriorations observed in obesity but their role is not yet completely understood.The first study consisted in giving a diet enriched in OFS to PPAR-a. knock-out mice (genetic model of obesity). 3 weeks of treatment with OFS led to a decrease in fasted glycemia and body weight gain but had no effect on lipid metabolism. We suggest that PPAR­ a expression might be necessaryfor OFS action on lipid homeostasis.In the second study a high-fat (HF) diet was administered to mice in order to induce obesity and diabetes. ln order to explore the role of Kupffer cells in this model, those cells were inhibited with gadolinium chloride (GdC13). After 4 weeks of treatment (HF diet versus control diet ± GdCIJ), GdCl3 inhibits Kupffer cells but causes an inflammatory state in the liver. However, it counteracts high-fat induced obesity and insulin-resistance. Indeed, it reduces body weight gain, the development of white adipose tissues and hepatic triglycerides steatosis. It also improves fasted glycemia and glucose response. Inhibition of Kupffer cel/s might decrease obesity and some associated metabolic disturbances, but its consequences on the overall and tissue specific immunity must be taken into account topropose those cells as a putative target in the control of metabolic syndrome. L'obésité, en augmentation constante dans les pays industrialisés, constitue aujourd'hui un problème majeur de santé publique. Elle favorise l 'apparition du syndrome métabolique (SM), caractérisé par de la dyslipidémie, de la stéatose, de l'hypertension et le développement du diabète de type 2. L'accumulation anormale de masse grasse va de pair avec la sécrétion d'acides gras et d'adipokines impliqués dans le développement de l'insulino-résistance et du SM. Mieux comprendre l 'implication de certaines cibles moléculaires et cellulaires dans l'accumulation de masse grasse et ses conséquences métaboliques permettra notamment de comprendre comment des approches thérapeutiques nouvelles (notamment des aliments fonctionnels) pourraient s'avérer utiles pour tenter d'enrayer l'évolution de ce fléau.Dans ce contexte, nous avons réalisé deux études in vivo afin de déterminer : -l'implication du récepteur nucléaire PPAR-o: dans les effets de l'oligofructose (OFS), un fructane non digestible fermenté dans le caeco-colon. PPAR-a est largement impliqué dans la prise alimentaire, le métabolisme lipidique et la réponse au glucose et l'OFS a déjà montré de nombreux effets bénéfiques dans divers modèles d'obésité chez les rongeurs.- le rôle des cellules de Kupffer dans le développement de l'obésité et des perturbations qui y sont associées. Ces macrophages hépatiques semblent impliqués dans les altérations hépatiques liées à l'obésité mais leur rôle n'est pas encore bien défini.La première étude consistait à administrer une diète enrichie en OFS à des souris invalidées pour le gène PPARo: (modèle d'obésité génétique). Trois semaines de traitement avec l'OFS ont permis de diminuer la glycémie à l'état nourri et le gain de poids corporel mais n'ont pas eu d'effet sur le métabolisme lipidique. Nous postulons que l'expression de PPARo: est peut­ être nécessaire à l'action de l'OFS sur ce dernier.Dans la deuxième étude, une diète « high-fat » (HF) a été administrée à des souris afin de les rendre obèses et diabétiques. Pour étudier le rôle des cellules de Kupffer dans ce modèle, nous avons inhibé celles-ci à l'aide de chlorure de gadolinium (GdCh). Après 4 semaines de traitement (diète HF versus diète contrôle ± GdCh), le GdCh inhibe bien les cellules de Kupffer mais provoque un état inflammatoire au niveau du foie. Cependant, il corrige l'obésité et l'insulino­ résistance induites par la diète HF : il diminue la prise de poids, le développement des tissus adipeux et le taux de triglycérides hépatiques et il améliore la glycémie à jeun et la réponse glycémique. L'inhibition des cellules de Kupffer semble donc positive d'un point de vue lllétabolique mais aurait un effet néfaste sur l 'état inflammatoire.

Obesity --- PPAR alpha --- Kupffer Cells

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Thyroid associated ophthalmopathy (TAO) is an autoimmune disorder associated to Graves’disease. In chronic phase, it is characterised by fibrosis and novo adipogenesis, but the mechanism is not yet clear. In this work, we have observed an extended infiltration of mast cells in TAO extraocular muscles and they certainly play a key role in the development of fibrotic and adipose tissues.
Muscular cells themselves have been poorly analysed up to now and are generally considered as intact, although TAO, as all autoimmune disorders, certainly involves oxidative stress. Indeed, we have observed an increased number of cells whose nuclei were labelled with caspase-6, a marker of cell apoptosis. Concomitantly, in TAO cases, the cytoplasmic expression of peroxiredoxines (PRDX5, PRDX3), known as antioxidant proteins was increased. As shown by immunohistochemistry and RT-PCR, adiponectin level was also increased in TAO, adiponectin being located in the cytoplasm of the muscular cells and of endothelial cells. PPARγ known to stimulate adiponectin expression is also detected at high level in the nuclei of muscular cells in cases of TAO. The upregulation of adiponectin and PPARγ could be linked to the antioxidant properties of both proteins.
In conclusion, extraocular muscular cells do possess a protective system against oxidative stress in autoimmune TAO

Antioxidants --- Oxidative Stress --- Adiponectin --- PPAR gamma --- Graves Ophthalmopathy --- Muscle Cells --- Satellite Cells, Skeletal Muscle --- Mice, Obese

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This eBook is a collection of articles from a Frontiers Research Topic. Frontiers Research Topics are very popular trademarks of the Frontiers Journals Series: they are collections of at least ten articles, all centered on a particular subject. With their unique mix of varied contributions from Original Research to Review Articles, Frontiers Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area! Find out more on how to host your own Frontiers Research Topic or contribute to one as an author by contacting the Frontiers Editorial Office: frontiersin.org/about/contact

Medicine --- Endocrinology --- obesity --- diabetes --- adipose tissue --- body composition --- TRPV1 - transient receptor potential vanilloid type 1 receptor --- PPAR gamma --- HIV --- hepatocyte growth factor (HGF)

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This eBook is a collection of articles from a Frontiers Research Topic. Frontiers Research Topics are very popular trademarks of the Frontiers Journals Series: they are collections of at least ten articles, all centered on a particular subject. With their unique mix of varied contributions from Original Research to Review Articles, Frontiers Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area! Find out more on how to host your own Frontiers Research Topic or contribute to one as an author by contacting the Frontiers Editorial Office: frontiersin.org/about/contact

Medicine --- Endocrinology --- obesity --- diabetes --- adipose tissue --- body composition --- TRPV1 - transient receptor potential vanilloid type 1 receptor --- PPAR gamma --- HIV --- hepatocyte growth factor (HGF) --- obesity --- diabetes --- adipose tissue --- body composition --- TRPV1 - transient receptor potential vanilloid type 1 receptor --- PPAR gamma --- HIV --- hepatocyte growth factor (HGF)

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Mounting evidence suggests a bidirectional relationship between metabolism and inflammation. Molecular crosstalk between these processes occurs at different levels with the participation of nuclear receptors, including peroxisome proliferator-activated receptors (PPARs). There are three PPAR isotypes, α, β/δ, and γ, which modulate metabolic and inflammatory pathways, making them key for the control of cellular, organ, and systemic processes. PPAR activity is governed by fatty acids and fatty acid derivatives, and by drugs used in clinics (glitazones and fibrates). The study of PPAR action, also modulated by post-translational modifications, has enabled extraordinary advances in the understanding of the multifaceted roles of these receptors in metabolism, energy homeostasis, and inflammation both in health and disease. This Special Issue of IJMS includes a broad range of basic and translational article, both original research and reviews, focused on the latest developments in the regulation of metabolic and/or inflammatory processes by PPARs in all organs and the microbiomes of different vertebrate species.

nuclear receptor --- gene transcription --- inflammation --- molecular docking --- PPARβ/δ --- lung --- pulmonary artery --- GW0742 --- GSK3787 --- docking --- lipopolysaccharide (LPS) --- PPARγ ligand --- coumarin --- fluorescent ligand --- screening --- crystal structure --- PPAR --- atopic dermatitis --- psoriasis --- metabolic reprograming --- glucose --- fatty acids --- mycobacteria --- M. tuberculosis --- M. leprae --- PPARs --- lipid droplets --- metabolic alterations --- hepatic damage --- nuclear factors --- pharmacological targets --- AMPK --- GDF15 --- insulin resistance --- type 2 diabetes mellitus --- peroxisome proliferator-activated receptor gamma (PPARγ) --- real-time PCR --- ELISA --- immunohistochemistry --- signaling pathway --- PPAR gamma --- brain --- neural stem cells --- infection --- neuroinflammation --- HIV --- Zika --- cytomegalovirus --- neurogenesis --- microglia --- liver damage --- toll-like receptor 4 --- P2Y2 receptor --- metabolic syndrome --- resveratrol --- quercetin --- PPARα --- peroxisome --- β-oxidation --- PPRE --- ligand --- coregulator --- micronutrients --- PPARα knockout --- adipose tissue --- browning --- lipid metabolism --- depression --- PPARg --- neuropathology --- corticotropin releasing hormone --- norepinephrine --- subgenual prefrontal cortex --- amygdala --- nucleus accumbens --- common carotid artery occlusion --- electroretinography --- fibroblast growth factor 21 --- pemafibrate --- peroxisome proliferator-activated receptor alpha --- retinal ischemia --- skeletal muscle --- substrate metabolism --- nonalcoholic fatty liver disease (NAFLD) --- sex dimorphism --- lipidomics --- hepatic sex-biased gene expression --- PPARγ --- pulmonary arterial hypertension --- TGFβ --- vascular injury --- proliferation --- kidney fibrosis --- pattern-recognition receptors --- phagocytosis --- nitric oxide synthase --- fenofibrate --- oleoylethanolamide --- palmitoylethanolamide --- cancer --- immunity --- obesity --- diabetes --- miRNA --- DNA methylation --- histone modification --- peroxisome-proliferator-activated receptor --- fatty acid oxidation --- doping control --- regulatory T cells --- exercise --- nuclear receptors --- nutrigenomics --- energy homeostasis --- dairy animals --- non-alcoholic fatty liver disease (NAFLD) --- non-alcoholic steatohepatitis (NASH) --- peroxisome proliferator-activated receptors (PPAR) --- bezafibrate --- fenofibric acid --- peroxisome proliferator-activated receptor --- dual/pan agonist --- X-ray crystallography --- n/a