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Bakker, W.* ; Imbernon, M.* ; Salinas, C.G.* ; Moro Chao, D.H.* ; Hassouna, R.* ; Morel, C.* ; Martin, C.* ; Leger, C.* ; Denis, R.G.P.* ; Castel, J.* ; Peter, A. ; Heni, M. ; Maetzler, W.* ; Nielsen, H.S.* ; Duquenne, M.* ; Schwaninger, M.* ; Lundh, S.* ; Johan Hogendorf, W.F.* ; Gangarossa, G.* ; Secher, A.* ; Hecksher-Sørensen, J.* ; Pedersen, T.Å.* ; Prévot, V.* ; Luquet, S.*

Acute changes in systemic glycemia gate access and action of GLP-1R agonist on brain structures controlling energy homeostasis.

Cell Rep. 41:111698 (2022)
Verlagsversion Forschungsdaten DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Therapies based on glucagon-like peptide-1 (GLP-1) long-acting analogs and insulin are often used in the treatment of metabolic diseases. Both insulin and GLP-1 receptors are expressed in metabolically relevant brain regions, suggesting a cooperative action. However, the mechanisms underlying the synergistic actions of insulin and GLP-1R agonists remain elusive. In this study, we show that insulin-induced hypoglycemia enhances GLP-1R agonists entry in hypothalamic and area, leading to enhanced whole-body fat oxidation. Mechanistically, this phenomenon relies on the release of tanycyctic vascular endothelial growth factor A, which is selectively impaired after calorie-rich diet exposure. In humans, low blood glucose also correlates with enhanced blood-to-brain passage of insulin, suggesting that blood glucose gates the passage other energy-related signals in the brain. This study implies that the preventing hyperglycemia is important to harnessing the full benefit of GLP-1R agonist entry in the brain and action onto lipid mobilization and body weight loss.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Brain Access ; Cp: Metabolism ; Diabetes ; Glucagon-like Peptide 1 Analogs ; Glycemic Control ; Metabolism ; Nutrient Partitioning ; Obesity ; Tanycyte
ISSN (print) / ISBN 2211-1247
e-ISSN 2211-1247
Zeitschrift Cell Reports
Quellenangaben Band: 41, Heft: 8, Seiten: , Artikelnummer: 111698 Supplement: ,
Verlag Cell Press
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Diabetes Research and Metabolic Diseases (IDM)