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@ARTICLE{Bakker:165605,
      author       = {Bakker, Wineke and Imbernon, Monica and Salinas, Casper
                      Gravesen and Moro Chao, Daniela Herrera and Hassouna, Rim
                      and Morel, Chloe and Martin, Claire and Leger, Caroline and
                      Denis, Raphael G P and Castel, Julien and Peter, Andreas and
                      Heni, Martin and Maetzler, Walter and Nielsen, Heidi Solvang
                      and Duquenne, Manon and Schwaninger, Markus and Lundh, Sofia
                      and Johan Hogendorf, Wouter Frederic and Gangarossa,
                      Giuseppe and Secher, Anna and Hecksher-Sørensen, Jacob and
                      Pedersen, Thomas Åskov and Prevot, Vincent and Luquet,
                      Serge},
      title        = {{A}cute changes in systemic glycemia gate access and action
                      of {GLP}-1{R} agonist on brain structures controlling energy
                      homeostasis.},
      journal      = {Cell reports},
      volume       = {41},
      number       = {8},
      issn         = {2211-1247},
      address      = {[New York, NY]},
      publisher    = {Elsevier},
      reportid     = {DZNE-2022-01738},
      pages        = {111698},
      year         = {2022},
      abstract     = {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.},
      keywords     = {Humans / Blood Glucose: metabolism / Vascular Endothelial
                      Growth Factor A: metabolism / Glucagon-Like Peptide 1:
                      metabolism / Insulin: metabolism / Homeostasis / Brain:
                      metabolism / CP: Metabolism (Other) / brain access (Other) /
                      diabetes (Other) / glucagon-like peptide 1 analogs (Other) /
                      glycemic control (Other) / metabolism (Other) / nutrient
                      partitioning (Other) / obesity (Other) / tanycyte (Other) /
                      Blood Glucose (NLM Chemicals) / Vascular Endothelial Growth
                      Factor A (NLM Chemicals) / Glucagon-Like Peptide 1 (NLM
                      Chemicals) / Insulin (NLM Chemicals)},
      cin          = {AG Maetzler},
      ddc          = {610},
      cid          = {I:(DE-2719)5000024},
      pnm          = {353 - Clinical and Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pmc          = {pmc:PMC9715912},
      pubmed       = {pmid:36417883},
      doi          = {10.1016/j.celrep.2022.111698},
      url          = {https://pub.dzne.de/record/165605},
}