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@ARTICLE{Makdissi:284345,
      author       = {Makdissi, Nikola and Hirschmann, Daria J and Frolov,
                      Aleksej and Sado, Inaam and Bennühr, Bastian and Nikolka,
                      Fabian and Cheng, Jingyuan and Blank-Stein, Nelli and Viola,
                      Maria Francesca and Yaghmour, Mohamed and Arnold, Philipp
                      and Bonaguro, Lorenzo and Becker, Matthias and Thiele,
                      Christoph and Meissner, Felix and Hiller, Karsten and Beyer,
                      Marc D and Mass, Elvira},
      title        = {{K}upffer cells control neonatal hepatic metabolism via
                      {I}gf1 signaling.},
      journal      = {Development},
      volume       = {153},
      number       = {2},
      issn         = {0022-0752},
      address      = {Cambridge},
      publisher    = {The Company of Biologists},
      reportid     = {DZNE-2026-00116},
      pages        = {dev204962},
      year         = {2026},
      abstract     = {During perinatal development, liver metabolism is tightly
                      regulated to ensure energy supply for the newborn. Before
                      birth, glycogen is stored in hepatocytes and later
                      metabolized to glucose, meeting neonatal energy demands.
                      Shortly after birth, lipogenesis begins, driven by
                      transcriptional activation of enzymes involved in fatty acid
                      oxidation. These processes are thought to be largely
                      regulated by systemic insulin and glucagon levels. However,
                      the role of liver-derived local factors in neonatal
                      hepatocyte metabolism remains unexplored. Kupffer cells
                      (KCs), the liver's resident macrophages, colonize the fetal
                      liver early in embryogenesis and support liver metabolism in
                      adulthood. Yet whether KCs influence neonatal hepatocyte
                      metabolism is unknown. Using conditional knockout mouse
                      models targeting macrophages, we demonstrate that yolk
                      sac-derived KCs play a crucial role in hepatocyte glycogen
                      storage and function by regulating the tricarboxylic acid
                      cycle, a role monocyte-derived KC-like cells cannot
                      substitute. Newborn pups lacking yolk sac-derived KCs
                      mobilize glycogen more rapidly, a process in part regulated
                      by insulin-like growth factor 1 (Igf1) production. Our
                      findings identify KCs as major source of Igf1, with local
                      production essential for balanced hepatocyte metabolism at
                      birth.},
      keywords     = {Animals / Insulin-Like Growth Factor I: metabolism /
                      Kupffer Cells: metabolism / Kupffer Cells: cytology / Liver:
                      metabolism / Liver: cytology / Hepatocytes: metabolism /
                      Mice / Signal Transduction / Animals, Newborn / Mice,
                      Knockout / Glycogen: metabolism / Yolk Sac: metabolism /
                      Yolk Sac: cytology / Citric Acid Cycle / Hepatocytes (Other)
                      / Igf1 (Other) / Kupffer cell (Other) / Liver development
                      (Other) / Macrophage (Other) / Insulin-Like Growth Factor I
                      (NLM Chemicals) / Glycogen (NLM Chemicals) / insulin-like
                      growth factor-1, mouse (NLM Chemicals)},
      cin          = {PRECISE / AG Beyer / AG Bonaguro / AG Becker},
      ddc          = {570},
      cid          = {I:(DE-2719)1013031 / I:(DE-2719)1013035 /
                      I:(DE-2719)1016005 / I:(DE-2719)5000079},
      pnm          = {352 - Disease Mechanisms (POF4-352) / 351 - Brain Function
                      (POF4-351) / 354 - Disease Prevention and Healthy Aging
                      (POF4-354)},
      pid          = {G:(DE-HGF)POF4-352 / G:(DE-HGF)POF4-351 /
                      G:(DE-HGF)POF4-354},
      experiment   = {EXP:(DE-2719)PRECISE-20190321},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41459815},
      doi          = {10.1242/dev.204962},
      url          = {https://pub.dzne.de/record/284345},
}