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Praticien-chercheur
8 articles scientifiques publiés — formation continue solide
Référence presse grand public
Cité 2 fois dans les médias — pédagogie reconnue
✨ Génération du profil synthétique IA en cours…
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Source : Google News (recherche par nom complet — homonymes possibles, vérifier le contenu).
📰 Actu.fr · 23/09/2019
<a href="https://news.google.com/rss/articles/CBMiywFBVV95cUxORmxkU3g3RHdwdzVySXN1c3pGby1PdjFjc3dMSHo2eDBWZUJNV2U0SllQaWFZQVdIRU1wZmx1bVVRT3ltT213TWktOHUyYmVrcktlWkRwM19tdWVneUZsSkZrTDVLSHlmczA1UHp6c0VEbWpzWUJOOGFpMExpWFk4bU5EVU5XM0dEdTFXWEFQaXppWjFHMXliZjlLaDNTNlNmemdTUkFWVWg2clYwT050VUx0elctMFF5VW
📰 Le Parisien · 28/03/2017
<a href="https://news.google.com/rss/articles/CBMi7wFBVV95cUxNRjQ3X2tqTS13TDVzWmIxUzFoRk14WTgtZ0tTNk1TbDZCbktnWWg0R0t1NG5pbHpjQVp5bmhpRHZoUWNWSl9iSUUtTDB5eWJNSF8wVl9PbllMUDNOMl9ZVzFITVJyZ0pacXRsczR1amNraFBwclRyU1I5UnV5LU9lMEpGS3JDSEFYN0xfUThwc1BCSTdIMGJHMlZkZm1iTGdhalYzcHI0ZEpLZGJKVVhEd1AwdVc5NTdpOE
Gut · 2013
Objective Non-alcoholic fatty liver disease (NAFLD) is prevalent among obese people and is considered the hepatic manifestation of metabolic syndrome. However, not all obese individuals develop NAFLD. Our objective was to demonstrate the role of the gut microbiota in NAFLD development using transplantation experiments in mice. Design Two donor C57BL/6J mice were selected on the basis of their responses to a high-fat diet (HFD). Although both mice displayed similar body weight gain, one mouse, called the ‘responder’, developed hyperglycaemia and had a high plasma concentration of pro-inflammatory cytokines. The other, called a ‘non-responder’, was normoglycaemic and had a lower level of systemic inflammation. Germ-free mice were colonised with intestinal microbiota from either the responder or the non-responder and then fed the same HFD. Results Mice that received microbiota from different donors developed comparable obesity on the HFD. The responder-receiver (RR) group developed fasting hyperglycaemia and insulinaemia, whereas the non-responder-receiver (NRR) group remained normoglycaemic. In contrast to NRR mice, RR mice developed hepatic macrovesicular steatosis, which was confirmed by a higher liver concentration of triglycerides and increased expression of genes involved in de-novo lipogenesis. Pyrosequencing of the 16S ribosomal RNA genes revealed that RR and NRR mice had distinct gut microbiota including differences at the phylum, genera and species levels. Conclusions Differences in microbiota composition can determine response to a HFD in mice. These results further demonstrate that the gut microbiota contributes to the development of NAFLD independently of obesity.
Gut · 2016
Objective There is substantial inter-individual diversity in the susceptibility of alcoholics to liver injury. Alterations of intestinal microbiota (IM) have been reported in alcoholic liver disease (ALD), but the extent to which they are merely a consequence or a cause is unknown. We aimed to demonstrate that a specific dysbiosis contributes to the development of alcoholic hepatitis (AH). Design We humanised germ-free and conventional mice using human IM transplant from alcoholic patients with or without AH. The consequences on alcohol-fed recipient mice were studied. Results A specific dysbiosis was associated with ALD severity in patients. Mice harbouring the IM from a patient with severe AH (sAH) developed more severe liver inflammation with an increased number of liver T lymphocyte subsets and Natural Killer T (NKT) lymphocytes, higher liver necrosis, greater intestinal permeability and higher translocation of bacteria than mice harbouring the IM from an alcoholic patient without AH (noAH). Similarly, CD45 + lymphocyte subsets were increased in visceral adipose tissue, and CD4 + T and NKT lymphocytes in mesenteric lymph nodes. The IM associated with sAH and noAH could be distinguished by differences in bacterial abundance and composition. Key deleterious species were associated with sAH while the Faecalibacterium genus was associated with noAH. Ursodeoxycholic acid was more abundant in faeces from noAH mice. Additionally, in conventional mice humanised with the IM from an sAH patient, a second subsequent transfer of IM from an noAH patient improved alcohol-induced liver lesions. Conclusions Individual susceptibility to ALD is substantially driven by IM. It may, therefore, be possible to prevent and manage ALD by IM manipulation.
Environmental microbiology · 2011
Summary The endogenous gut microbiota affects the host in many ways. Prebiotics should favour beneficial intestinal microbes and thus improve host health. In this study, we investigated how a novel class of potential prebiotic long‐chain arabinoxylans (LC‐AX) and the well‐established prebiotic inulin (IN) modulate the gut microbiota of humanized rats. Six weeks after axenic rats were inoculated with a human faecal microbiota, their colonic microbiota was similar to this inoculum (∼ 70%), whereas their caecal microbiota was enriched with Verrucomicrobia and Firmicutes concomitant with lower abundance of Bacteroidetes . Moreover, different Bifidobacterium species colonized the lumen ( B. adolescentis ) and mucus ( B. longum and B. bifidum ). Both LC‐AX and IN increased SCFA levels and induced a shift from acetate towards health‐promoting propionate and butyrate respectively. By applying a high‐resolution phylogenetic micro‐array (HITChip) at the site of fermentation (caecum), IN and LC‐AX were shown to stimulate bacterial groups with known butyrate‐producers ( Roseburia intestinalis , Eubacterium rectale , Anaerostipes caccae ) and bifidobacteria ( B. longum ) respectively. Prebiotic administration also resulted in lower caecal abundances of the mucin‐degrading Akkermansia muciniphila and potentially more mucin production by the host. Both factors might explain the increased caecal mucin levels for LC‐AX (threefold) and IN (sixfold). These mucins were degraded along the colon, resulting in high faecal abundances of Akkermansia muciniphila for LC‐AX and especially IN‐treated rats. Finally, the microbial changes caused an adaptation period for the host with less weight gain, after which the host fine‐tuned the interaction with this altered microbiota. Our results demonstrate that next to IN, LC‐AX are promising prebiotic compounds by stimulating production of health‐promoting metabolites by specific microbes in the proximal regions. Further, prebiotic supplementation shifted mucin degradation to distal regions, where mucin‐degraders may produce beneficial metabolites (e.g. propionate by Akkermansia muciniphila ), so that prebiotics may potentially improve gut health along the entire length of the intestine.
Source PubMed · Recherche par auteur (homonymes possibles, vérifier l'affiliation).
Molecular nutrition & food research · 2020 · Journal Article
Busnelli M, Manzini S, Jablaoui A, Bruneau A, et al.
mBio · 2020 · Journal Article
Fei N, Bruneau A, Zhang X, Wang R, et al.
Nutrients · 2020 · Journal Article
Safari Z, Bruneau A, Monnoye M, Mariadassou M, et al.
Scientific reports · 2016 · Journal Article
Rabot S, Membrez M, Blancher F, Berger B, et al.
Gut · 2016 · Journal Article
Llopis M, Cassard AM, Wrzosek L, Boschat L, et al.
Gut · 2013 · Journal Article
Le Roy T, Llopis M, Lepage P, Bruneau A, et al.
PloS one · 2013 · Journal Article
Respondek F, Gerard P, Bossis M, Boschat L, et al.
Environmental microbiology · 2011 · Comparative Study
Van den Abbeele P, Gérard P, Rabot S, Bruneau A, et al.
Nutrients · 2020 · Journal Article
Safari Z, Bruneau A, Monnoye M, Mariadassou M, et al.