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@ARTICLE{Jennemann:153913,
      author       = {R. Jennemann$^*$ and S. Kaden$^*$ and M. Volz$^*$ and V.
                      Nordström$^*$ and S. Herzer$^*$ and R. Sandhoff$^*$ and
                      H.-J. Gröne$^*$},
      title        = {{G}angliosides {M}odulate {I}nsulin {S}ecretion by
                      {P}ancreatic {B}eta-{C}ells under {G}lucose {S}tress.},
      journal      = {Glycobiology},
      volume       = {30},
      number       = {9},
      issn         = {1460-2423},
      address      = {Oxford},
      publisher    = {Oxford Univ. Press},
      reportid     = {DKFZ-2020-00523},
      pages        = {722-734},
      year         = {2020},
      note         = {2020 Aug 20;30(9):722-734#EA:A411#LA:G130#},
      abstract     = {In pancreatic beta cells the entry of glucose and
                      downstream signaling for insulin release is regulated by the
                      glucose transporter 2 (Glut2) in rodents. Dysfunction of the
                      insulin-signaling cascade may lead to diabetes mellitus.
                      Gangliosides, sialic acid-containing glycosphingolipids
                      (GSLs), have been reported to modulate the function of
                      several membrane proteins. Murine islets express
                      predominantly sialylated GSLs, particularly the simple
                      gangliosides GM3 and GD3 having a potential modulatory role
                      in Glut2 activity. Conditional, tamoxifen-inducible gene
                      targeting in pancreatic islets has now shown that mice
                      lacking the glucosylceramide synthase (Ugcg), which
                      represents the rate-limiting enzyme in GSL-biosynthesis,
                      displayed impaired glucose uptake and showed reduced insulin
                      secretion. Consequently, mice with pancreatic GSL deficiency
                      had higher blood glucose levels than respective controls
                      after intraperitoneal glucose application. High fat diet
                      feeding enhanced this effect. GSL-deficient islets did not
                      show apoptosis or ER-stress and displayed a normal
                      ultra-structure. Their insulin content, size and number was
                      similar as in control islets. Isolated beta cells from GM3
                      synthase null mice unable to synthesize GM3 and GD3 also
                      showed lower glucose uptake than respective control cells,
                      corroborating the results obtained from the cell-specific
                      model. We conclude that in particular the negatively charged
                      gangliosides GM3 and GD3 of beta cells positively influence
                      Glut2 function to adequately respond to high glucose loads.},
      cin          = {A411 / G130},
      ddc          = {610},
      cid          = {I:(DE-He78)A411-20160331 / 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:32149357},
      doi          = {10.1093/glycob/cwaa022},
      url          = {https://inrepo02.dkfz.de/record/153913},
}