Добірка наукової літератури з теми "Maladie du foie gras non-alcoolique (NAFLD) – Recherche"
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Дисертації з теми "Maladie du foie gras non-alcoolique (NAFLD) – Recherche"
Burz, Sebastian D. "Implication du microbiote intestinal humain dans l‘évolution des hépatopathies métaboliques non liées à l’alcoolisme (NAFLD)." Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASA004.
Повний текст джерелаNon-alcoholic fatty liver diseases (NAFLD) include a spectrum of liver diseases ranging from fatty liver (NAFL), going through fibrosis (NASH), then cirrhosis in the absence of alcohol consumption, viral infection or other identified causes, and sometimes the development of hepatocellular carcinoma (HCC). Due to its high prevalence, up to a quarter of the general European population and its harmful consequences on the health of those who suffer from it, NAFLD represent a major public health issue.This liver disease has been associated with changes in gut microbiota and metabolic pathways in which this microbiota is involved. In mice, gut microbiota contributes to the worsening or protection of this disease.The goal of the thesis is to determine whether in humans the gut microbiota contributes also to this individual susceptibility observed in NAFLD mice.A complete standardized procedure for preparing, storing and managing human fecal transplants is developed and implemented (Burz et al., 2019).Specific pathogens free mice (SPF), pretreated with a cocktail of antibiotics, were colonized with microbiota derived from an healthy individual or patients at different stages of NAFLD. Then these mice were challenged with a high fructose, high fat diet in order to explore the effect of installed human microbiota on the onset and progression of induced NAFLD.This project made it possible to demonstrate, through the transfer of the human fecal microbiota, with constant food energy intake, the transfer of overweight. The human NAFL fecal microbiota worsens liver steatosis in mice, but mitigates liver and caecal inflammation.This thesis sheds additional light on the impact of gut microbiota in the establishment of the natural pathophysiology of NAFLD, especially during the early phase of the disease. The project also generated additional knowledge that could be developed in future projects in order to establish therapeutic strategies targeting gut microbiota. This set constitutes an important achievement in a very competitive research field, which generates major interest for food and pharmaceutical industries, and thus supports the international development of the different partners of the project
Le, Roy Tiphaine. "Implication du microbiote intestinal dans l’insulino-résistance et les pathologies hépatiques associées à l’obésité, étude sur modèle murin." Electronic Thesis or Diss., Paris, AgroParisTech, 2012. http://www.theses.fr/2012AGPT0016.
Повний текст джерелаObesity predisposes people to several severe pathologies, including type 2 diabetes and NAFLD (Non Alcoholic Fatty Liver Disease). Such pathologies are characterized by insulin resistance and systemic low grade inflammation. Recently, it has been established that such pathologies are associated to a gut microbiota dysbiosis. Moreover, recent studies in mice and human indicate that modulation of gut microbiota composition has beneficial effects on people suffering type 2 diabetes and/or NAFLD. Otherwise, it has been showed that germ-free mice remain lean, normo-glycemic and sensitive to insulin when fed a high-fat diet.The aim of this study was i) to decipher to what extent the pathogenesis of insulin resistance and NAFLD depends on the presence or absence of gut microbiota, ii) to determine if the predisposition to metabolic disorders in an obesity context can be transferred via gut microbiota transplantation.We first compared the response of germ-free and conventional mice to high fat diet. Indeed, germ-free mice appeared to be resistant to high-fat diet-induced obesity and insulin resistance. However, germ-freeness only partially protects against diet-induced steatosis, that is to say accumulation of triglycerides in hepatocytes. In conventional mice, high-fat diet induced an increase of the hepatic expression of genes involved in lipogenesis. The inverse phenomenon was observed in germ-free mice. In order to study the liver inflammation, we isolated and cultivated liver macrophages from the two groups of mice. As in conventional mice, high-fat diet induced an increased secretion of pro-inflammatory cytokines by germ-free mice liver macrophages. However, germ-free mice macrophages remained sensitive to LPS stimulation, which was not observed in the conventional mice group. This results demonstrates that being devoid of gut microbiota deeply alters the immunological and metabolic responses to high-fat diet. Therefore, differences in gut microbiota composition could explain the differences of susceptibility in diet-induced insulin-resistance and NAFLD.Then, we colonised two groups of germ-free mice with the gut microbiota of two conventional mice the responses of which to high-fat diet were discrepant. The two donors mice presented different levels of fasting glycemia and HOMA-IR index despite a similar body weight. Both groups of colonised mice developped comparable obesity but different degrees of fasting glycemia and insulin resistance. Levels of steatosis and hepatic expression of genes involved in lipogenesis were as well different in the two groups of colonised mice. Hence the results clearly show that the gut microbiota is the cause of the predisposition to diet-induced insulin resistance and hepatic steatosis. Gut microbiota analysis revealed a higher proportion of lactic acid bacteria, Atopobium, Bacteroides and Akkermansia muciniphila in receiver mice resistant to diet-induced insulin resistance and steatosis, which allow us to hypothesize a protective effect of these bacteria in diet-induced metabolic disorders
Deprince, Audrey. "Rôle de l’Apolipoprotéine F dans le métabolisme des lipides : impact sur le développement de la stéatose hépatique non alcoolique." Thesis, Université de Lille (2018-2021), 2021. https://pepite-depot.univ-lille.fr/ToutIDP/EDBSL/2021/2021LILUS063.pdf.
Повний текст джерелаNon-Alcoholic Fatty Liver Disease (NAFLD) is a chronic, progressive disease which includes a spectrum of disease states ranging from isolated hepatic steatosis to steatohepatitis (or NASH). These changes in the liver have a significant impact on overall physiology and indicate higher risk of mortality from cardiovascular disease and hepatocellular carcinoma. However, the molecular mechanisms driving NAFLD evolution to NASH remain poorly understood. Through an unbiased transcriptomic analysis, we identified Apolipoprotein F (ApoF) whose expression is inversely correlated with steatosis and reduced ~ 50% in subjects with NASH. ApoF is secreted exclusively from the liver and found associated with high-density (HDL) and low-density lipoprotein (LDL) particles. Previous functional studies of ApoF have shown that ApoF favors reverse cholesterol transport in mice. These results suggest ApoF could affect NAFLD development and/or its cardiovascular complications.However, the precise role of ApoF in lipoprotein metabolism remains poorly understood. In this project, we have identified a new role for ApoF. Our results show that overexpression of APOF in mice is associated with a decrease in fasting plasma triglycerides (TG) levels by promoting both VLDL secretion and clearance of TG-rich particles via an increase in their hepatic uptake, probably through activation of the SREBP2 pathway.Subsequently, we sought to determine the impact of modulating hepatic ApoF expression on the development of NAFLD in mice fed with a high fat diet supplemented with sucrose and cholesterol, which induces NASH. Surprisingly, our results show that raising the level of hepatic APOF in the context of NAFLD may rather be deleterious. We observed an aggravation of hepatic inflammation and unfavorable changes in plasma lipids (reduced HDL-C and increased LDL-C) in mice overexpressing APOF compared to GFP after being fed the NASH-inducing diet. Similarly, total deletion of ApoF does not seem to accelerate the development of the disease. Thus, our results suggest that the decrease in hepatic APOF expression in NAFLD patients may be a compensatory mechanism to prevent a deleterious effect of ApoF activity. However, further studies are needed to confirm the role of ApoF in the development of NAFLD
Belot, Audrey. "Régulation du métabolisme du fer et nouvelles stratégies thérapeutiques." Thesis, Toulouse 3, 2020. http://www.theses.fr/2020TOU30009.
Повний текст джерелаIron homeostasis is a paradox. It is both essential for living organisms but deleterious in excess. Iron balance is maintained by hepcidin, a hormone produced by the liver. Matriptase-2 is an inhibitor of hepcidin expression. The absence of matriptase-2 causes IRIDA, a disease characterized by a severe anemia and an iron deficiency. In this study, I showed in mice that a hepcidin-suppressing molecule corrects the iron deficiency and the anemia of IRIDA. Thus, this molecule could be used in therapy. In this work, I was also interested in the role of iron in fatty liver disease which can progress in some cases to a more severe stage for which no treatments are available. I have shown that hepcidin production is increased in this disease, resulting in liver iron retention that could be an aggravating factor. The characterization of this dysregulation has led to the identification of a promising new therapeutic target to prevent the disease progression
Smati-Grangeon, Sarra. "Influence du sexe dans la susceptibilité aux hépatopathies métaboliques." Thesis, Toulouse 3, 2019. http://www.theses.fr/2019TOU30213.
Повний текст джерелаNon Alcoholic Fatty Liver Disease (NAFLD), ranging from steatosis to steatohepatitis (NASH), is the most common liver disease and a major public health issue worldwide. There are strong clinical and preclinical evidence for sexual dimorphism. The establishment of reliable animal models is essential to understand the mechanisms underlying such gender specific susceptibility to the disease. We aimed at identifying a mouse model of NAFLD that replicates at best the sexual dimorphism observed in humans. We tested different hypercaloric diets: High-Fat Diet (HFD), Choline Deficient HFD, Western Diet enriched with cholesterol and co-administered or not with drinking water containing glucose and fructose in male and female C57BL/6J mice (n=12/group). Histological, biochemical, transcriptomic and metabolomic analyses were performed. The Western Diet induces a strong dimorphic phenotype for the onset of NASH. Males develop major steatosis associated with severe inflammation and fibrosis whereas females show much less steatosis. Both sexes develop obesity and have impaired glucose tolerance. In contrast, insulin resistance is more severe in males than in females. Finally, liver transcriptome analysis highlights contrasted gene expression profiles between males and females in response to the different diets. Gene network analysis suggest that nuclear receptors are influential in this sexual dimorphic response to dietary challenges. Among nuclear receptors, ERalpha is the major effector of estrogen signaling in the liver. We tested the western diet in male and female mice in absence of ERalpha in hepatocytes. This deletion did not cause significant changes in hepatic phenotype in response to western diet in males and females. Another nuclear receptor has been studied, PPARalpha plays a central role in lipid metabolism and is protective against NAFLD. In the absence of PPARalpha in hepatocytes, fatty acid catabolism is defective during fasting in male mice. Therefore, to investigate whether hepatocyte PPARalpha activity shows sexual dimorphism, we tested the effect of fasting in female mice. In vivo experiments in mice with a hepatocyte specific knock-out of PPARalpha reveal that fasting induces similar PPARalpha-dependent ketogenesis in mice from both sexes.[...]
Chavez, Talavera Oscar Manuel. "Rôle des acides biliaires dans la physiopathologie de l'obésité, la résistance à l'insuline, le diabète de type 2, la stéatose hépatique non alcoolique et dans le contexte de la chirurgie bariatrique Bile Acid Control of Metabolism and Inflammation in Obesity, Type 2 Diabetes, Dyslipidemia, and Nonalcoholic Fatty Liver Disease Bile Acid Alterations in Nonalcoholic Fatty Liver Disease, Obesity, Insulin Resistance and Type 2 Diabetes: What Do the Human Studies Tell?” Bile acids associate with glucose metabolism, but do not predict conversion to diabetes Bile acid alterations are associated with insulin resistance, but not with NASH in obese subjects Roux-en-Y gastric bypass increases systemic but not portal bile acid concentrations by decreasing hepatic bile acid uptake in minipigs The functional relevance of bile acids in the improvement of HDL-mediated endothelial protection after bariatric surgery Metabolic effects of bile acid sequestration: impact on cardiovascular risk factors." Thesis, Lille, 2019. http://www.theses.fr/2019LILUS057.
Повний текст джерелаIn addition to their role in the solubilization of dietary lipids, bile acids are signaling molecules regulating their own metabolism, glucose and lipid homeostasis, energy expenditure, cardiovascular function and inflammation via the activation of the Farnesoid X Receptor (FXR) and the Takeda G protein coupled Receptor 5 (TGR5). Indeed, changes in bile acid concentrations are associated with metabolic diseases and therefore they are candidates to participate in the pathophysiology of these diseases or predict their progression.In the first part of this thesis, we studied bile acid changes in the context of obesity, insulin resistance, type 2 diabetes and non-alcoholic steatohepatitis. We demonstrated that bile acids are correlated with glucose homeostasis in humans, but that they are not predictors for the progression from prediabetes to type 2 diabetes in a longitudinal cohort study.In the second part of this thesis, we studied the bile acids in the context of bariatric surgery. Our results showed that bariatric surgery reduces the hepatic recapture of certain bile acids, causing them to increase in the systemic circulation. Additionally, we showed that it is not the bile limb but the common limb the one responsible for metabolic changes after bariatric surgery in the minipig. Finally, we showed in humans that bile acids linked to high-density lipoproteins (HDL) increase after bariatric surgery, and that this increase is correlated with the restoration of their vasoprotective functions