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Yu, Q.* ; Gamayun, I.* ; Wartenberg, P.* ; Zhang, Q. ; Qiao, S.* ; Kusumakshi, S.* ; Candlish, S.* ; Götz, V.* ; Wen, S.* ; Das, D.* ; Wyatt, A.* ; Wahl, V.* ; Ectors, F.* ; Kattler, K.* ; Yildiz, D.* ; Prévot, V.* ; Schwaninger, M.* ; Ternier, G.* ; Giacobini, P.* ; Ciofi, P.* ; Müller, T.D. ; Boehm, U.*

Bitter taste cells in the ventricular walls of the murine brain regulate glucose homeostasis.

Nat. Commun. 14:1588 (2023)
Verlagsversion DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
The median eminence (ME) is a circumventricular organ at the base of the brain that controls body homeostasis. Tanycytes are its specialized glial cells that constitute the ventricular walls and regulate different physiological states, however individual signaling pathways in these cells are incompletely understood. Here, we identify a functional tanycyte subpopulation that expresses key taste transduction genes including bitter taste receptors, the G protein gustducin and the gustatory ion channel TRPM5 (M5). M5 tanycytes have access to blood-borne cues via processes extended towards diaphragmed endothelial fenestrations in the ME and mediate bidirectional communication between the cerebrospinal fluid and blood. This subpopulation responds to metabolic signals including leptin and other hormonal cues and is transcriptionally reprogrammed upon fasting. Acute M5 tanycyte activation induces insulin secretion and acute diphtheria toxin-mediated M5 tanycyte depletion results in impaired glucose tolerance in diet-induced obese mice. We provide a cellular and molecular framework that defines how bitter taste cells in the ME integrate chemosensation with metabolism.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Arcuate Nucleus; Messenger-rna; Food-intake; Tanycytes; Ablation; Protein; Mice; Expression; Plasticity; Receptors
ISSN (print) / ISBN 2041-1723
e-ISSN 2041-1723
Zeitschrift Nature Communications
Quellenangaben Band: 14, Heft: 1, Seiten: , Artikelnummer: 1588 Supplement: ,
Verlag Nature Publishing Group
Verlagsort London
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Diabetes and Obesity (IDO)
Förderungen European Research Council (ERC)
DFG and Saarland University
Deutsche Forschungsgemeinschaft (DFG)