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<p>Pancreatic β-cells maintain glucose homeostasis by secreting insulin in response to rising blood glucose, a process fueled by mitochondrial ATP production. Iron, a core cofactor in the electron transport chain, is essential for this metabolic coupling. While the cytotoxic effects of iron overload are well known, the role of iron sufficiency during β-cell development remains unclear. Here, we identify a maturation-dependent requirement for iron in mouse and human β-cells. Using chemical chelation and genetic disruption of transferrin receptor (TFRC)-mediated uptake, we show that immature β-cells depend on iron during metabolic transition to functional maturity. Iron restriction at this stage impairs oxidative metabolism and compromises survival. In contrast, mature β-cells remain resilient to iron depletion, revealing a developmental switch in iron dependency. These findings establish iron as a key metabolic cue in β-cell development and suggest strategies to generate fully functional stem cell-derived β-cells for diabetes modeling and cell replacement therapy.</p>

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Iron deficiency induces maturation-dependent loss of pancreatic β-cells

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年2月16日

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  • Annelore Van Mulders,
  • Lien Willems,
  • Sophie Coenen,
  • Stephanie Bourgeois,
  • Xiaoyan Yi,
  • Yue Tong,
  • Gunter Leuckx,
  • Yves Heremans,
  • Julie Pierreux,
  • Laure Degroote,
  • Toshiaki Sawatani,
  • Chiara Vinci,
  • Gamze Ates,
  • Ann Massie,
  • Françoise Carlotti,
  • Eelco de Koning,
  • Thomas Mandrup-Poulsen,
  • Clara Zelinsky,
  • Steven Goderis,
  • Bart Ghesquière,
  • Raphael Scharfmann,
  • Miriam Cnop,
  • Nico De Leu,
  • Willem Staels

摘要

Pancreatic β-cells maintain glucose homeostasis by secreting insulin in response to rising blood glucose, a process fueled by mitochondrial ATP production. Iron, a core cofactor in the electron transport chain, is essential for this metabolic coupling. While the cytotoxic effects of iron overload are well known, the role of iron sufficiency during β-cell development remains unclear. Here, we identify a maturation-dependent requirement for iron in mouse and human β-cells. Using chemical chelation and genetic disruption of transferrin receptor (TFRC)-mediated uptake, we show that immature β-cells depend on iron during metabolic transition to functional maturity. Iron restriction at this stage impairs oxidative metabolism and compromises survival. In contrast, mature β-cells remain resilient to iron depletion, revealing a developmental switch in iron dependency. These findings establish iron as a key metabolic cue in β-cell development and suggest strategies to generate fully functional stem cell-derived β-cells for diabetes modeling and cell replacement therapy.