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  1. Article ; Online: Prenatal stress induces changes in PAR2- and M3-dependent regulation of colon primitive cells.

    Berger, Mathieu / Guiraud, Laura / Dumas, Alexia / Sagnat, David / Payros, Gaëlle / Rolland, Corinne / Vergnolle, Nathalie / Deraison, Céline / Cenac, Nicolas / Racaud-Sultan, Claire

    American journal of physiology. Gastrointestinal and liver physiology

    2022  Volume 323, Issue 6, Page(s) G609–G626

    Abstract: Prenatal stress is associated with a high risk of developing adult intestinal pathologies, such as irritable bowel syndrome, chronic inflammation, and cancer. Although epithelial stem cells and progenitors have been implicated in intestinal ... ...

    Abstract Prenatal stress is associated with a high risk of developing adult intestinal pathologies, such as irritable bowel syndrome, chronic inflammation, and cancer. Although epithelial stem cells and progenitors have been implicated in intestinal pathophysiology, how prenatal stress could impact their functions is still unknown. We have investigated the proliferative and differentiation capacities of primitive cells using epithelial crypts isolated from colons of adult male and female mice whose mothers have been stressed during late gestation. Our results show that stem cell/progenitor proliferation and differentiation in vitro are negatively impacted by prenatal stress in male progeny. This is promoted by a reinforcement of the negative proliferative/differentiation control by the protease-activated receptor 2 (PAR2) and the muscarinic receptor 3 (M3), two G protein-coupled receptors present in the crypt. Conversely, prenatal stress does not change in vitro proliferation of colon primitive cells in female progeny. Importantly, this maintenance is associated with a functional switch in the M3 negative control of colonoid growth, becoming proliferative after prenatal stress. In addition, the proliferative role of PAR2 specific to females is maintained under prenatal stress, even though PAR2-targeted stress signals Dusp6 and activated GSK3β are increased, reaching the levels of males. An epithelial serine protease could play a critical role in the activation of the survival kinase GSK3β in colonoids from prenatally stressed female progeny. Altogether, our results show that following prenatal stress, colon primitive cells cope with stress through sexually dimorphic mechanisms that could pave the way to dysregulated crypt regeneration and intestinal pathologies.
    MeSH term(s) Male ; Female ; Mice ; Animals ; Pregnancy ; Receptor, PAR-2/genetics ; Glycogen Synthase Kinase 3 beta ; Colon ; Stem Cells ; Receptors, G-Protein-Coupled
    Chemical Substances Receptor, PAR-2 ; Glycogen Synthase Kinase 3 beta (EC 2.7.11.1) ; Receptors, G-Protein-Coupled
    Language English
    Publishing date 2022-10-25
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 603840-2
    ISSN 1522-1547 ; 0193-1857
    ISSN (online) 1522-1547
    ISSN 0193-1857
    DOI 10.1152/ajpgi.00061.2022
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.89: Show issues Location:
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  2. Article ; Online: Bacteria-derived long chain fatty acid exhibits anti-inflammatory properties in colitis.

    Pujo, Julien / Petitfils, Camille / Le Faouder, Pauline / Eeckhaut, Venessa / Payros, Gaelle / Maurel, Sarah / Perez-Berezo, Teresa / Van Hul, Matthias / Barreau, Frederick / Blanpied, Catherine / Chavanas, Stephane / Van Immerseel, Filip / Bertrand-Michel, Justine / Oswald, Eric / Knauf, Claude / Dietrich, Gilles / Cani, Patrice D / Cenac, Nicolas

    Gut

    2020  Volume 70, Issue 6, Page(s) 1088–1097

    Abstract: Objective: Data from clinical research suggest that certain probiotic bacterial strains have the potential to modulate colonic inflammation. Nonetheless, these data differ between studies due to the probiotic bacterial strains used and the poor ... ...

    Abstract Objective: Data from clinical research suggest that certain probiotic bacterial strains have the potential to modulate colonic inflammation. Nonetheless, these data differ between studies due to the probiotic bacterial strains used and the poor knowledge of their mechanisms of action.
    Design: By mass-spectrometry, we identified and quantified free long chain fatty acids (LCFAs) in probiotics and assessed the effect of one of them in mouse colitis.
    Results: Among all the LCFAs quantified by mass spectrometry in
    Conclusion: The production of C18-3OH by bacteria could be one of the mechanisms implicated in the anti-inflammatory properties of probiotics. The production of LCFA-3OH by bacteria could be implicated in the microbiota/host interactions.
    MeSH term(s) Animals ; Bacteroidetes ; Caco-2 Cells ; Cell Membrane Permeability ; Chemokine CXCL1/genetics ; Colitis/chemically induced ; Colitis/drug therapy ; Colitis/metabolism ; Dextran Sulfate ; Epithelial Cells/physiology ; Escherichia coli/metabolism ; Firmicutes/metabolism ; Gastrointestinal Microbiome/physiology ; Gene Expression/drug effects ; Humans ; Interleukin-1beta/genetics ; Intestinal Mucosa/metabolism ; Mass Spectrometry ; Mice ; Oligosaccharides/pharmacology ; PPAR gamma/genetics ; PPAR gamma/metabolism ; Pancreatitis-Associated Proteins/genetics ; Permeability ; Peyer's Patches ; Prebiotics ; Probiotics/chemistry ; Stearates/analysis ; Stearates/metabolism ; Stearates/therapeutic use ; Zonula Occludens-1 Protein/genetics
    Chemical Substances Chemokine CXCL1 ; Cxcl1 protein, mouse ; IL1B protein, mouse ; Interleukin-1beta ; Oligosaccharides ; PPAR gamma ; Pancreatitis-Associated Proteins ; Pparg protein, mouse ; Prebiotics ; Reg3g protein, mouse ; Stearates ; Tjp1 protein, mouse ; Zonula Occludens-1 Protein ; fructooligosaccharide ; 3-hydroxyoctadecanoate (17773-30-7) ; Dextran Sulfate (9042-14-2)
    Language English
    Publishing date 2020-09-25
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80128-8
    ISSN 1468-3288 ; 0017-5749
    ISSN (online) 1468-3288
    ISSN 0017-5749
    DOI 10.1136/gutjnl-2020-321173
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 160: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  3. Article ; Online: Identification of bacterial lipopeptides as key players in IBS.

    Petitfils, Camille / Maurel, Sarah / Payros, Gaelle / Hueber, Amandine / Agaiz, Bahija / Gazzo, Géraldine / Marrocco, Rémi / Auvray, Frédéric / Langevin, Geoffrey / Motta, Jean-Paul / Floch, Pauline / Tremblay-Franco, Marie / Galano, Jean-Marie / Guy, Alexandre / Durand, Thierry / Lachambre, Simon / Durbec, Anaëlle / Hussein, Hind / Decraecker, Lisse /
    Bertrand-Michel, Justine / Saoudi, Abdelhadi / Oswald, Eric / Poisbeau, Pierrick / Dietrich, Gilles / Melchior, Chloe / Boeckxstaens, Guy / Serino, Matteo / Le Faouder, Pauline / Cenac, Nicolas

    Gut

    2022  Volume 72, Issue 5, Page(s) 939–950

    Abstract: Objectives: Clinical studies revealed that early-life adverse events contribute to the development of IBS in adulthood. The aim of our study was to investigate the relationship between prenatal stress (PS), gut microbiota and visceral hypersensitivity ... ...

    Abstract Objectives: Clinical studies revealed that early-life adverse events contribute to the development of IBS in adulthood. The aim of our study was to investigate the relationship between prenatal stress (PS), gut microbiota and visceral hypersensitivity with a focus on bacterial lipopeptides containing γ-aminobutyric acid (GABA).
    Design: We developed a model of PS in mice and evaluated, in adult offspring, visceral hypersensitivity to colorectal distension (CRD), colon inflammation, barrier function and gut microbiota taxonomy. We quantified the production of lipopeptides containing GABA by mass spectrometry in a specific strain of bacteria decreased in PS, in PS mouse colons, and in faeces of patients with IBS and healthy volunteers (HVs). Finally, we assessed their effect on PS-induced visceral hypersensitivity.
    Results: Prenatally stressed mice of both sexes presented visceral hypersensitivity, no overt colon inflammation or barrier dysfunction but a gut microbiota dysbiosis. The dysbiosis was distinguished by a decreased abundance of
    Conclusion: PS impacts the gut microbiota composition and metabolic function in adulthood. The reduced capacity of the gut microbiota to produce GABA lipopeptides could be one of the mechanisms linking PS and visceral hypersensitivity in adulthood.
    MeSH term(s) Male ; Female ; Mice ; Animals ; Irritable Bowel Syndrome/microbiology ; Dysbiosis ; Gastrointestinal Microbiome ; Feces/microbiology ; Inflammation
    Language English
    Publishing date 2022-10-14
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80128-8
    ISSN 1468-3288 ; 0017-5749
    ISSN (online) 1468-3288
    ISSN 0017-5749
    DOI 10.1136/gutjnl-2022-328084
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 160: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  4. Article ; Online: Blood microbiota dysbiosis is associated with the onset of cardiovascular events in a large general population: the D.E.S.I.R. study.

    Amar, Jacques / Lange, Céline / Payros, Gaëlle / Garret, Celine / Chabo, Chantal / Lantieri, Olivier / Courtney, Michael / Marre, Michel / Charles, Marie Aline / Balkau, Beverley / Burcelin, Rémy

    PloS one

    2013  Volume 8, Issue 1, Page(s) e54461

    Abstract: Aim: We recently described a human blood microbiome and a connection between this microbiome and the onset of diabetes. The aim of the current study was to assess the association between blood microbiota and incident cardiovascular disease.: Methods ... ...

    Abstract Aim: We recently described a human blood microbiome and a connection between this microbiome and the onset of diabetes. The aim of the current study was to assess the association between blood microbiota and incident cardiovascular disease.
    Methods and results: D.E.S.I.R. is a longitudinal study with the primary aim of describing the natural history of the metabolic syndrome and its complications. Participants were evaluated at inclusion and at 3-, 6-, and 9-yearly follow-up visits. The 16S ribosomal DNA bacterial gene sequence, that is common to the vast majority of bacteria (Eubac) and a sequence that mostly represents Proteobacteria (Pbac), were measured in blood collected at baseline from 3936 participants. 73 incident cases of acute cardiovascular events, including 30 myocardial infarctions were recorded. Eubac was positively correlated with Pbac (r = 0.59; P<0.0001). In those destined to have cardiovascular complications, Eubac was lower (0.14±0.26 vs 0.12±0.29 ng/µl; P = 0.02) whereas a non significant increase in Pbac was observed. In multivariate Cox analysis, Eubac was inversely correlated with the onset of cardiovascular complications, (hazards ratio 0.50 95% CI 0.35-0.70) whereas Pbac (1.56, 95%CI 1.12-2.15) was directly correlated.
    Conclusion: Pbac and Eubac were shown to be independent markers of the risk of cardiovascular disease. This finding is evidence for the new concept of the role played by blood microbiota dysbiosis on atherothrombotic disease. This concept may help to elucidate the relation between bacteria and cardiovascular disease.
    MeSH term(s) Adult ; Age of Onset ; Aged ; Bacteria/genetics ; Bacteria/isolation & purification ; Biomarkers/blood ; Cardiovascular Diseases/complications ; Cardiovascular Diseases/diagnosis ; Cardiovascular Diseases/epidemiology ; Cardiovascular Diseases/microbiology ; Female ; France/epidemiology ; Humans ; Incidence ; Longitudinal Studies ; Male ; Metabolic Syndrome/complications ; Metabolic Syndrome/diagnosis ; Metabolic Syndrome/epidemiology ; Metabolic Syndrome/microbiology ; Metagenome/genetics ; Middle Aged ; Proportional Hazards Models ; Proteobacteria/genetics ; Proteobacteria/isolation & purification ; RNA, Ribosomal, 16S/blood ; RNA, Ribosomal, 16S/genetics ; RNA, Ribosomal, 16S/isolation & purification ; Risk
    Chemical Substances Biomarkers ; RNA, Ribosomal, 16S
    Language English
    Publishing date 2013-01-25
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0054461
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Lipid-induced peroxidation in the intestine is involved in glucose homeostasis imbalance in mice.

    Serino, Matteo / Waget, Aurélie / Marsollier, Nicolas / Masseboeuf, Myriam / Payros, Gaëlle / Kabani, Catherine / Denom, Jessica / Lacombe, Amélie / Thiers, Jean-Claude / Negre-Salvayre, Anne / Luquet, Serge / Burcelin, Rémy / Cruciani-Guglielmacci, Céline / Magnan, Christophe

    PloS one

    2011  Volume 6, Issue 6, Page(s) e21184

    Abstract: Background: Daily variations in lipid concentrations in both gut lumen and blood are detected by specific sensors located in the gastrointestinal tract and in specialized central areas. Deregulation of the lipid sensors could be partly involved in the ... ...

    Abstract Background: Daily variations in lipid concentrations in both gut lumen and blood are detected by specific sensors located in the gastrointestinal tract and in specialized central areas. Deregulation of the lipid sensors could be partly involved in the dysfunction of glucose homeostasis. The study aimed at comparing the effect of Medialipid (ML) overload on insulin secretion and sensitivity when administered either through the intestine or the carotid artery in mice.
    Methodology/principal findings: An indwelling intragastric or intracarotid catheter was installed in mice and ML or an isocaloric solution was infused over 24 hours. Glucose and insulin tolerance and vagus nerve activity were assessed. Some mice were treated daily for one week with the anti-lipid peroxidation agent aminoguanidine prior to the infusions and tests. The intestinal but not the intracarotid infusion of ML led to glucose and insulin intolerance when compared with controls. The intestinal ML overload induced lipid accumulation and increased lipid peroxidation as assessed by increased malondialdehyde production within both jejunum and duodenum. These effects were associated with the concomitant deregulation of vagus nerve. Administration of aminoguanidine protected against the effects of lipid overload and normalized glucose homeostasis and vagus nerve activity.
    Conclusions/significance: Lipid overload within the intestine led to deregulation of gastrointestinal lipid sensing that in turn impaired glucose homeostasis through changes in autonomic nervous system activity.
    MeSH term(s) Animals ; Glucose/metabolism ; Guanidines/pharmacology ; Homeostasis ; Insulin Resistance ; Intestinal Mucosa/metabolism ; Intestines/drug effects ; Lipid Peroxidation/drug effects ; Mice ; Oxidative Stress
    Chemical Substances Guanidines ; Glucose (IY9XDZ35W2) ; pimagedine (SCQ4EZQ113)
    Language English
    Publishing date 2011-06-16
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0021184
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Physiological and pharmacological mechanisms through which the DPP-4 inhibitor sitagliptin regulates glycemia in mice.

    Waget, Aurélie / Cabou, Cendrine / Masseboeuf, Myriam / Cattan, Pierre / Armanet, Mattieu / Karaca, Mélis / Castel, Julien / Garret, Celine / Payros, Gaëlle / Maida, Adriano / Sulpice, Thierry / Holst, Jens J / Drucker, Daniel J / Magnan, Christophe / Burcelin, Rémy

    Endocrinology

    2011  Volume 152, Issue 8, Page(s) 3018–3029

    Abstract: Inhibition of dipeptidyl peptidase-4 (DPP-4) activity improves glucose homeostasis through a mode of action related to the stabilization of the active forms of DPP-4-sensitive hormones such as the incretins that enhance glucose-induced insulin secretion. ...

    Abstract Inhibition of dipeptidyl peptidase-4 (DPP-4) activity improves glucose homeostasis through a mode of action related to the stabilization of the active forms of DPP-4-sensitive hormones such as the incretins that enhance glucose-induced insulin secretion. However, the DPP-4 enzyme is highly expressed on the surface of intestinal epithelial cells; hence, the role of intestinal vs. systemic DPP-4 remains unclear. To analyze mechanisms through which the DPP-4 inhibitor sitagliptin regulates glycemia in mice, we administered low oral doses of the DPP-4 inhibitor sitagliptin that selectively reduced DPP-4 activity in the intestine. Glp1r(-/-) and Gipr(-/-) mice were studied and glucagon-like peptide (GLP)-1 receptor (GLP-1R) signaling was blocked by an i.v. infusion of the corresponding receptor antagonist exendin (9-39). The role of the dipeptides His-Ala and Tyr-Ala as DPP-4-generated GLP-1 and glucose-dependent insulinotropic peptide (GIP) degradation products was studied in vivo and in vitro on isolated islets. We demonstrate that very low doses of oral sitagliptin improve glucose tolerance and plasma insulin levels with selective reduction of intestinal but not systemic DPP-4 activity. The glucoregulatory action of sitagliptin was associated with increased vagus nerve activity and was diminished in wild-type mice treated with the GLP-1R antagonist exendin (9-39) and in Glp1r(-/-) and Gipr(-/-) mice. Furthermore, the dipeptides liberated from GLP-1 (His-Ala) and GIP (Tyr-Ala) deteriorated glucose tolerance, reduced insulin, and increased portal glucagon levels. The predominant mechanism through which DPP-4 inhibitors regulate glycemia involves local inhibition of intestinal DPP-4 activity, activation of incretin receptors, reduced liberation of bioactive dipeptides, and activation of the gut-to-pancreas neural axis.
    MeSH term(s) Adult ; Animals ; Blood Glucose/analysis ; Dipeptides/pharmacology ; Dipeptidyl Peptidase 4/physiology ; Dipeptidyl-Peptidase IV Inhibitors/pharmacology ; Glucagon/metabolism ; Glucagon-Like Peptide-1 Receptor ; Glucose Tolerance Test ; Humans ; Insulin/metabolism ; Insulin Secretion ; Male ; Mice ; Mice, Inbred C57BL ; Middle Aged ; Pyrazines/pharmacology ; Receptors, Gastrointestinal Hormone/physiology ; Receptors, Glucagon/physiology ; Sitagliptin Phosphate ; Triazoles/pharmacology ; Vagus Nerve/physiology
    Chemical Substances Blood Glucose ; Dipeptides ; Dipeptidyl-Peptidase IV Inhibitors ; GLP1R protein, human ; Glp1r protein, mouse ; Glucagon-Like Peptide-1 Receptor ; Insulin ; Pyrazines ; Receptors, Gastrointestinal Hormone ; Receptors, Glucagon ; Triazoles ; histidinoalanine (16874-75-2) ; Glucagon (9007-92-5) ; gastric inhibitory polypeptide receptor (D6H00MV7K8) ; Dipeptidyl Peptidase 4 (EC 3.4.14.5) ; Sitagliptin Phosphate (TS63EW8X6F)
    Language English
    Publishing date 2011-06-14
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 427856-2
    ISSN 1945-7170 ; 0013-7227
    ISSN (online) 1945-7170
    ISSN 0013-7227
    DOI 10.1210/en.2011-0286
    Database MEDical Literature Analysis and Retrieval System OnLINE

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