45 research outputs found

    The oral lipid sensor GPR120 is not indispensable for the orosensory detectionof dietary lipids in the mouse

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    International audienceImplication of the long-chain fatty acid (LCFA) receptor GPR120, also termed free fatty acid receptor 4 (FFAR4), in the taste-guided preference for lipids is a matter of debate. To further unravel the role of GPR120 in the "taste of fat", the present study was conducted on GPR120-null mice and their wild-type littermates. Using a combination of morphological (i.e. immunohistochemical staining of circumvallate papillae - CVP), behavioral (i.e. two-bottle preference tests, licking tests and conditioned taste aversion) and functional studies (i.e. calcium imaging in freshly isolated taste bud cells - TBC), we show that absence of GPR120 in oral cavity was not associated with changes in i) the gross anatomy of CVP, ii) the LCFA-mediated increases in [Ca2+]i, iii) the preference for oily and LCFA solutions and iv) the conditioned avoidance of LCFA solutions. In contrast, the rise in [Ca2+]i triggered by grifolic acid (GA), a specific GPR120 agonist, was dramatically curtailed when GPR120 gene was lacking. Taken together these data demonstrate that activation of lingual GPR120 and preference for fat are disconnected, suggesting that GPR120 expressed in TBC is not absolutely required for the oral fat detection in the mouse

    Douleur au point de ponction de péridurale dans le post-partum : proposition thérapeutique en acupuncture

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    Acupuncture obstétricaleCe mémoire rend compte d’une étude comparative d’un traitement avec ou sans acupuncture sur les douleurs au point de ponction de péridurale dans le post-partum. L’étude montre que le traitement par acupuncture aide à la diminution du niveau de douleur et permet surtout de faire disparaître plus rapidement cette douleur sur le long term

    Liraglutide for patients with non-alcoholic steatohepatitis

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    International audienc

    Browning Epicardial Adipose Tissue: Friend or Foe?

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    International audienceThe epicardial adipose tissue (EAT) is the visceral fat depot of the heart which is highly plastic and in direct contact with myocardium and coronary arteries. Because of its singular proximity with the myocardium, the adipokines and pro-inflammatory molecules secreted by this tissue may directly affect the metabolism of the heart and coronary arteries. Its accumulation, measured by recent new non-invasive imaging modalities, has been prospectively associated with the onset and progression of coronary artery disease (CAD) and atrial fibrillation in humans. Recent studies have shown that EAT exhibits beige fat-like features, and express uncoupling protein 1 (UCP-1) at both mRNA and protein levels. However, this thermogenic potential could be lost with age, obesity and CAD. Here we provide an overview of the physiological and pathophysiological relevance of EAT and further discuss whether its thermogenic properties may serve as a target for obesity therapeutic management with a specific focus on the role of immune cells in this beiging phenomenon

    COVID-19 and Obesity: Role of Ectopic Visceral and Epicardial Adipose Tissues in Myocardial Injury

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    In March 2020, the WHO declared coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a global pandemic. Obesity was soon identified as a risk factor for poor prognosis, with an increased risk of intensive care admissions and mechanical ventilation, but also of adverse cardiovascular events. Obesity is associated with adipose tissue, chronic low-grade inflammation, and immune dysregulation with hypertrophy and hyperplasia of adipocytes and overexpression of pro-inflammatory cytokines. However, to implement appropriate therapeutic strategies, exact mechanisms must be clarified. The role of white visceral adipose tissue, increased in individuals with obesity, seems important, as a viral reservoir for SARS-CoV-2 via angiotensin-converting enzyme 2 (ACE2) receptors. After infection of host cells, the activation of pro-inflammatory cytokines creates a setting conducive to the "cytokine storm" and macrophage activation syndrome associated with progression to acute respiratory distress syndrome. In obesity, systemic viral spread, entry, and prolonged viral shedding in already inflamed adipose tissue may spur immune responses and subsequent amplification of a cytokine cascade, causing worse outcomes. More precisely, visceral adipose tissue, more than subcutaneous fat, could predict intensive care admission; and lower density of epicardial adipose tissue (EAT) could be associated with worse outcome. EAT, an ectopic adipose tissue that surrounds the myocardium, could fuel COVID-19-induced cardiac injury and myocarditis, and extensive pneumopathy, by strong expression of inflammatory mediators that could diffuse paracrinally through the vascular wall. The purpose of this review is to ascertain what mechanisms may be involved in unfavorable prognosis among COVID-19 patients with obesity, especially cardiovascular events, emphasizing the harmful role of excess ectopic adipose tissue, particularly EAT

    A chronic LPS-induced low-grade inflammation fails to reproduce in lean mice the impairment of preference for oily solution found in diet-induced obese mice

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    IF 3.188 (2017)International audienceDiet-induced obesity (DIO) is associated with a decreased oral fat detection in rodents. This alteration has been explained by an impairment of the lipid-mediated signaling in taste bud cells (TBC). However, factors responsible for this defect remain elusive. Diet rich in saturated fatty acids is known to elicit a metabolic inflammation by promoting intestinal permeation to lipopolysaccharides (LPS), Gram-negative bacteria-derived endotoxins. To determine whether a local inflammation of the gustatory tissue might explain the obese-induced impairment of the oro-sensory detection of lipids, mice were subjected to a DIO protocol. Using a combination of behavioral tests, transcriptomic analyses of gustatory papillae and biochemical assays, we have found that i) DIO elicits a pro-inflammatory genic profile in the circum-vallate papillae (CVP), known to house the highest density of lingual taste buds, ii) NFkB, a key player of inflammatory process, might play a role in this transcriptomic pattern, iii) plasma LPS levels are negatively correlated with the preference for oily solution, and iv) a chronic infusion of LPS at a level similar to that found in DIO mice is not sufficient to alter the spontaneous preference for fat in lean mice. Taken together these data bring the demonstration that a saturated high fat diet elicits an inflammatory response at the level of peripheral gustatory pathway and a LPS-induced low-grade endotoxemia alone does not explain the change in the preference for dietary lipids observed in DIO mice

    Exenatide decreases ectopic fat accumulation but have no impact on myocardial function and perfusion in patients with obesity and type 2 diabetes

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    International audienceThe objective of the study is to assess the impact of Exenatide on endothelial reactivity, and change in ectopic fat and cardiac function. This study included 44 patients (mean 52 years) randomized to Exenatide or reference treatment. Magnetic resonance imaging was used to assess ectopic fat accumulation, coronary vasoreactivity and cardiac function. 16-weeks of Exenatide treatement resulted in a significant improvement in glycemic control and a significant reduction of both epicardial fat and hepatic steatosis. However, we found no effect of Exenatide on myocardial function. In addition, one-week of exenatide treatment had only a modest effect on vascular reactivity, albeit non-significant

    Exenatide decreases ectopic fat accumulation but have no impact on myocardial function and perfusion in patients with obesity and type 2 diabetes

    No full text
    International audienceThe objective of the study is to assess the impact of Exenatide on endothelial reactivity, and change in ectopic fat and cardiac function. This study included 44 patients (mean 52 years) randomized to Exenatide or reference treatment. Magnetic resonance imaging was used to assess ectopic fat accumulation, coronary vasoreactivity and cardiac function. 16-weeks of Exenatide treatement resulted in a significant improvement in glycemic control and a significant reduction of both epicardial fat and hepatic steatosis. However, we found no effect of Exenatide on myocardial function. In addition, one-week of exenatide treatment had only a modest effect on vascular reactivity, albeit non-significant
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