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  1. Book ; Online ; Thesis: The role of metabolite receptors in tumor progression

    Brandenburger, Isabell [Verfasser] / Steinhilber, Dieter [Gutachter] / Offermanns, Stefan [Gutachter]

    2020  

    Author's details Isabell Brandenburger ; Gutachter: Dieter Steinhilber, Stefan Offermanns
    Keywords Medizin, Gesundheit ; Medicine, Health
    Subject code sg610
    Language English
    Publisher Universitätsbibliothek Johann Christian Senckenberg
    Publishing place Frankfurt am Main
    Document type Book ; Online ; Thesis
    Database Digital theses on the web

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  2. Article ; Online: 20-HETE promotes glucose-stimulated insulin secretion in an autocrine manner through FFAR1.

    Tunaru, Sorin / Bonnavion, Remy / Brandenburger, Isabell / Preussner, Jens / Thomas, Dominique / Scholich, Klaus / Offermanns, Stefan

    Nature communications

    2018  Volume 9, Issue 1, Page(s) 177

    Abstract: The long-chain fatty acid receptor FFAR1 is highly expressed in pancreatic β-cells. Synthetic FFAR1 agonists can be used as antidiabetic drugs to promote glucose-stimulated insulin secretion (GSIS). However, the physiological role of FFAR1 in β-cells ... ...

    Abstract The long-chain fatty acid receptor FFAR1 is highly expressed in pancreatic β-cells. Synthetic FFAR1 agonists can be used as antidiabetic drugs to promote glucose-stimulated insulin secretion (GSIS). However, the physiological role of FFAR1 in β-cells remains poorly understood. Here we show that 20-HETE activates FFAR1 and promotes GSIS via FFAR1 with higher potency and efficacy than dietary fatty acids such as palmitic, linoleic, and α-linolenic acid. Murine and human β-cells produce 20-HETE, and the ω-hydroxylase-mediated formation and release of 20-HETE is strongly stimulated by glucose. Pharmacological inhibition of 20-HETE formation and blockade of FFAR1 in islets inhibits GSIS. In islets from type-2 diabetic humans and mice, glucose-stimulated 20-HETE formation and 20-HETE-dependent stimulation of GSIS are strongly reduced. We show that 20-HETE is an FFAR1 agonist, which functions as an autocrine positive feed-forward regulator of GSIS, and that a reduced glucose-induced 20-HETE formation contributes to inefficient GSIS in type-2 diabetes.
    MeSH term(s) Adult ; Animals ; Autocrine Communication/drug effects ; COS Cells ; Cell Line ; Cell Line, Tumor ; Cells, Cultured ; Cercopithecus aethiops ; Diabetes Mellitus, Type 2/genetics ; Diabetes Mellitus, Type 2/metabolism ; Female ; Glucose/pharmacology ; Humans ; Hydroxyeicosatetraenoic Acids/blood ; Hydroxyeicosatetraenoic Acids/metabolism ; Hydroxyeicosatetraenoic Acids/pharmacology ; Insulin/metabolism ; Insulin Secretion ; Insulin-Secreting Cells/drug effects ; Insulin-Secreting Cells/metabolism ; Male ; Mice, Knockout ; Mice, Obese ; Middle Aged ; Receptors, G-Protein-Coupled/agonists ; Receptors, G-Protein-Coupled/genetics ; Receptors, G-Protein-Coupled/metabolism ; Young Adult
    Chemical Substances FFAR1 protein, human ; Hydroxyeicosatetraenoic Acids ; Insulin ; Receptors, G-Protein-Coupled ; 20-hydroxy-5,8,11,14-eicosatetraenoic acid (79551-86-3) ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2018-01-12
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2041-1723
    ISSN (online) 2041-1723
    DOI 10.1038/s41467-017-02539-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Cysteinyl leukotrienes and acetylcholine are biliary tuft cell cotransmitters.

    Keshavarz, Maryam / Faraj Tabrizi, Schayan / Ruppert, Anna-Lena / Pfeil, Uwe / Schreiber, Yannick / Klein, Jochen / Brandenburger, Isabell / Lochnit, Günter / Bhushan, Sudhanshu / Perniss, Alexander / Deckmann, Klaus / Hartmann, Petra / Meiners, Mirjam / Mermer, Petra / Rafiq, Amir / Winterberg, Sarah / Papadakis, Tamara / Thomas, Dominique / Angioni, Carlo /
    Oberwinkler, Johannes / Chubanov, Vladimir / Gudermann, Thomas / Gärtner, Ulrich / Offermanns, Stefan / Schütz, Burkhard / Kummer, Wolfgang

    Science immunology

    2022  Volume 7, Issue 69, Page(s) eabf6734

    Abstract: The gallbladder stores bile between meals and empties into the duodenum upon demand and is thereby exposed to the intestinal microbiome. This exposure raises the need for antimicrobial factors, among them, mucins produced by cholangiocytes, the dominant ... ...

    Abstract The gallbladder stores bile between meals and empties into the duodenum upon demand and is thereby exposed to the intestinal microbiome. This exposure raises the need for antimicrobial factors, among them, mucins produced by cholangiocytes, the dominant epithelial cell type in the gallbladder. The role of the much less frequent biliary tuft cells is still unknown. We here show that propionate, a major metabolite of intestinal bacteria, activates tuft cells via the short-chain free fatty acid receptor 2 and downstream signaling involving the cation channel transient receptor potential cation channel subfamily M member 5. This results in corelease of acetylcholine and cysteinyl leukotrienes from tuft cells and evokes synergistic paracrine effects upon the epithelium and the gallbladder smooth muscle, respectively. Acetylcholine triggers mucin release from cholangiocytes, an epithelial defense mechanism, through the muscarinic acetylcholine receptor M3. Cysteinyl leukotrienes cause gallbladder contraction through their cognate receptor CysLTR1, prompting emptying and closing. Our results establish gallbladder tuft cells as sensors of the microbial metabolite propionate, initiating dichotomous innate defense mechanisms through simultaneous release of acetylcholine and cysteinyl leukotrienes.
    MeSH term(s) Acetylcholine/metabolism ; Epithelial Cells/metabolism ; Leukotrienes ; Propionates
    Chemical Substances Leukotrienes ; Propionates ; Acetylcholine (N9YNS0M02X)
    Language English
    Publishing date 2022-03-04
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2470-9468
    ISSN (online) 2470-9468
    DOI 10.1126/sciimmunol.abf6734
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Lactate released by inflammatory bone marrow neutrophils induces their mobilization via endothelial GPR81 signaling.

    Khatib-Massalha, Eman / Bhattacharya, Suditi / Massalha, Hassan / Biram, Adi / Golan, Karin / Kollet, Orit / Kumari, Anju / Avemaria, Francesca / Petrovich-Kopitman, Ekaterina / Gur-Cohen, Shiri / Itkin, Tomer / Brandenburger, Isabell / Spiegel, Asaf / Shulman, Ziv / Gerhart-Hines, Zachary / Itzkovitz, Shalev / Gunzer, Matthias / Offermanns, Stefan / Alon, Ronen /
    Ariel, Amiram / Lapidot, Tsvee

    Nature communications

    2020  Volume 11, Issue 1, Page(s) 3547

    Abstract: Neutrophils provide first line of host defense against bacterial infections utilizing glycolysis for their effector functions. How glycolysis and its major byproduct lactate are triggered in bone marrow (BM) neutrophils and their contribution to ... ...

    Abstract Neutrophils provide first line of host defense against bacterial infections utilizing glycolysis for their effector functions. How glycolysis and its major byproduct lactate are triggered in bone marrow (BM) neutrophils and their contribution to neutrophil mobilization in acute inflammation is not clear. Here we report that bacterial lipopolysaccharides (LPS) or Salmonella Typhimurium triggers lactate release by increasing glycolysis, NADPH-oxidase-mediated reactive oxygen species and HIF-1α levels in BM neutrophils. Increased release of BM lactate preferentially promotes neutrophil mobilization by reducing endothelial VE-Cadherin expression, increasing BM vascular permeability via endothelial lactate-receptor GPR81 signaling. GPR81
    MeSH term(s) Animals ; Bone Marrow/blood supply ; Bone Marrow Cells/immunology ; Bone Marrow Cells/metabolism ; Disease Models, Animal ; Endothelium, Vascular/metabolism ; Female ; Humans ; Lactic Acid/metabolism ; Lipopolysaccharides/immunology ; Male ; Mice ; Mice, Knockout ; Neutrophils/immunology ; Neutrophils/metabolism ; Receptors, G-Protein-Coupled/genetics ; Receptors, G-Protein-Coupled/metabolism ; Salmonella Infections/immunology ; Salmonella Infections/microbiology ; Salmonella typhimurium/immunology ; Signal Transduction/immunology
    Chemical Substances Hcar1 protein, mouse ; Lipopolysaccharides ; Receptors, G-Protein-Coupled ; Lactic Acid (33X04XA5AT)
    Language English
    Publishing date 2020-07-15
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-020-17402-2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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