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@ARTICLE{Schumacher:140821,
      author       = {D. Schumacher and J. Morgenstern and Y. Oguchi and N. Volk
                      and S. Kopf and J. B. Groener and P. P. Nawroth$^*$ and T.
                      Fleming and M. Freichel},
      title        = {{C}ompensatory mechanisms for methylglyoxal detoxification
                      in experimental $\&$ clinical diabetes.},
      journal      = {Molecular metabolism},
      volume       = {18},
      issn         = {2212-8778},
      address      = {Oxford [u.a.]},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2018-01585},
      pages        = {143-152},
      year         = {2018},
      abstract     = {The deficit of Glyoxalase I (Glo1) and the subsequent
                      increase in methylglyoxal (MG) has been reported to be one
                      the five mechanisms by which hyperglycemia causes diabetic
                      late complications. Aldo-keto reductases (AKR) have been
                      shown to metabolize MG; however, the relative contribution
                      of this superfamily to the detoxification of MG in vivo,
                      particularly within the diabetic state, remains
                      unknown.CRISPR/Cas9-mediated genome editing was used to
                      generate a Glo1 knock-out (Glo1-/-) mouse line.
                      Streptozotocin was then applied to investigate metabolic
                      changes under hyperglycemic conditions.Glo1-/- mice were
                      viable and showed no elevated MG or MG-H1 levels under
                      hyperglycemic conditions. It was subsequently found that the
                      enzymatic efficiency of various oxidoreductases in the liver
                      and kidney towards MG were increased in the Glo1-/- mice.
                      The functional relevance of this was supported by the
                      altered distribution of alternative detoxification products.
                      Furthermore, it was shown that MG-dependent AKR activity is
                      a potentially clinical relevant pathway in human patients
                      suffering from diabetes.These data suggest that in the
                      absence of GLO1, AKR can effectively compensate to prevent
                      the accumulation of MG. The combination of metabolic,
                      enzymatic, and genetic factors, therefore, may provide a
                      better means of identifying patients who are at risk for the
                      development of late complications caused by elevated levels
                      of MG.},
      cin          = {A170},
      ddc          = {610},
      cid          = {I:(DE-He78)A170-20160331},
      pnm          = {311 - Signalling pathways, cell and tumor biology
                      (POF3-311)},
      pid          = {G:(DE-HGF)POF3-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30287091},
      doi          = {10.1016/j.molmet.2018.09.005},
      url          = {https://inrepo02.dkfz.de/record/140821},
}