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@ARTICLE{Okun:168147,
      author       = {J. G. Okun and P. M. Rusu and A. Y. Chan and Y. Wu and Y.
                      W. Yap and T. Sharkie and J. Schumacher$^*$ and K. V.
                      Schmidt and K. M. Roberts-Thomson and R. D. Russell and A.
                      Zota and S. Hille and A. Jungmann and L. Maggi$^*$ and Y.
                      Lee and M. Blüher and S. Herzig$^*$ and M. A. Keske and M.
                      Heikenwälder$^*$ and O. J. Müller and A. J. Rose$^*$},
      title        = {{L}iver alanine catabolism promotes skeletal muscle atrophy
                      and hyperglycaemia in type 2 diabetes.},
      journal      = {Nature metabolism},
      volume       = {3},
      number       = {3},
      issn         = {2522-5812},
      address      = {[London]},
      publisher    = {Springer Nature},
      reportid     = {DKFZ-2021-00712},
      pages        = {394 - 409},
      year         = {2021},
      note         = {Division of Molecular Metabolic Control#EA:A170#},
      abstract     = {Both obesity and sarcopenia are frequently associated in
                      ageing, and together may promote the progression of related
                      conditions such as diabetes and frailty. However, little is
                      known about the pathophysiological mechanisms underpinning
                      this association. Here we show that systemic alanine
                      metabolism is linked to glycaemic control. We find that
                      expression of alanine aminotransferases is increased in the
                      liver in mice with obesity and diabetes, as well as in
                      humans with type 2 diabetes. Hepatocyte-selective silencing
                      of both alanine aminotransferase enzymes in mice with
                      obesity and diabetes retards hyperglycaemia and reverses
                      skeletal muscle atrophy through restoration of skeletal
                      muscle protein synthesis. Mechanistically, liver alanine
                      catabolism driven by chronic glucocorticoid and glucagon
                      signalling promotes hyperglycaemia and skeletal muscle
                      wasting. We further provide evidence for amino acid-induced
                      metabolic cross-talk between the liver and skeletal muscle
                      in ex vivo experiments. Taken together, we reveal a
                      metabolic inter-tissue cross-talk that links skeletal muscle
                      atrophy and hyperglycaemia in type 2 diabetes.},
      cin          = {F180 / A170},
      ddc          = {610},
      cid          = {I:(DE-He78)F180-20160331 / I:(DE-He78)A170-20160331},
      pnm          = {316 - Infektionen, Entzündung und Krebs (POF4-316)},
      pid          = {G:(DE-HGF)POF4-316},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:33758419},
      doi          = {10.1038/s42255-021-00369-9},
      url          = {https://inrepo02.dkfz.de/record/168147},
}