Nature Communications (Jul 2022)

Hepatic non-parenchymal S100A9-TLR4-mTORC1 axis normalizes diabetic ketogenesis

  • Gloria Ursino,
  • Giorgio Ramadori,
  • Anna Höfler,
  • Soline Odouard,
  • Pryscila D. S. Teixeira,
  • Florian Visentin,
  • Christelle Veyrat-Durebex,
  • Giulia Lucibello,
  • Raquel Firnkes,
  • Serena Ricci,
  • Claudia R. Vianna,
  • Lin Jia,
  • Mirjam Dirlewanger,
  • Philippe Klee,
  • Joel K. Elmquist,
  • Johannes Roth,
  • Thomas Vogl,
  • Valérie M. Schwitzgebel,
  • François R. Jornayvaz,
  • Andreas Boland,
  • Roberto Coppari

DOI
https://doi.org/10.1038/s41467-022-31803-5
Journal volume & issue
Vol. 13, no. 1
pp. 1 – 17

Abstract

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Excess ketogenesis can lead to ketoacidosis, a serious complication in patients with diabetes. Here the authors report an insulin independent pathway, the hepatic nonparenchymal S100A9-TLR4-mTORC1 axis, that is able to normalize diabetic ketogenesis and pre-clinical data to suggest potential for development of S100A9 based adjunctive therapy to insulin.