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@ARTICLE{Hasan:154149,
      author       = {S. S. Hasan$^*$ and M. Jabs$^*$ and J. Taylor$^*$ and L.
                      Wiedmann$^*$ and T. Leibing and V. Nordström$^*$ and G.
                      Federico$^*$ and L. P. Roma and C. Carlein and G. Wolff and
                      B. Ekim-Üstünel and M. Brune and I. Moll$^*$ and F.
                      Tetzlaff$^*$ and H.-J. Gröne$^*$ and T. Fleming and C.
                      Géraud and S. Herzig and P. P. Nawroth and A. Fischer$^*$},
      title        = {{E}ndothelial {N}otch signaling controls insulin transport
                      in muscle.},
      journal      = {EMBO molecular medicine},
      volume       = {12},
      number       = {4},
      issn         = {1757-4676},
      address      = {Heidelberg},
      publisher    = {EMBO Press},
      reportid     = {DKFZ-2020-00610},
      pages        = {e09271},
      year         = {2020},
      note         = {#EA:A270#LA:A270#2020 Apr 7;12(4):e09271},
      abstract     = {The role of the endothelium is not just limited to acting
                      as an inert barrier for facilitating blood transport.
                      Endothelial cells (ECs), through expression of a repertoire
                      of angiocrine molecules, regulate metabolic demands in an
                      organ-specific manner. Insulin flux across the endothelium
                      to muscle cells is a rate-limiting process influencing
                      insulin-mediated lowering of blood glucose. Here, we
                      demonstrate that Notch signaling in ECs regulates insulin
                      transport to muscle. Notch signaling activity was higher in
                      ECs isolated from obese mice compared to non-obese.
                      Sustained Notch signaling in ECs lowered insulin sensitivity
                      and increased blood glucose levels. On the contrary,
                      EC-specific inhibition of Notch signaling increased insulin
                      sensitivity and improved glucose tolerance and glucose
                      uptake in muscle in a high-fat diet-induced insulin
                      resistance model. This was associated with increased
                      transcription of Cav1, Cav2, and Cavin1, higher number of
                      caveolae in ECs, and insulin uptake rates, as well as
                      increased microvessel density. These data imply that Notch
                      signaling in the endothelium actively controls insulin
                      sensitivity and glucose homeostasis and may therefore
                      represent a therapeutic target for diabetes.},
      cin          = {A270 / G130},
      ddc          = {610},
      cid          = {I:(DE-He78)A270-20160331 / I:(DE-He78)G130-20160331},
      pnm          = {311 - Signalling pathways, cell and tumor biology
                      (POF3-311)},
      pid          = {G:(DE-HGF)POF3-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:32187826},
      doi          = {10.15252/emmm.201809271},
      url          = {https://inrepo02.dkfz.de/record/154149},
}