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<p>Maintaining blood glucose homeostasis during fasting and feeding is crucial for the prevention of dysregulation that can lead to either hypo- or hyperglycaemia. Here we identified feimin, encoded by a gene with a previously unknown function (<i>B230219D22Rik</i> in mice, <i>C5orf24</i> in humans), as a key modulator of glucose homeostasis. Feimin is secreted from skeletal muscle during feeding and binds to its receptor, receptor protein tyrosine kinase Mer (MERTK), promoting glucose uptake and inhibiting glucose production by activation of AKT. Administration of feimin and insulin synergistically improves blood glucose homeostasis in both normal and diabetic mice. Notably, a specific single nucleotide polymorphism (rs7604639, G&gt;A) within the <i>MERTK</i> gene, causing an amino acid substitution (R466K) within the feimin–MERTK binding region, leads to reduced association with feimin and elevated postprandial blood glucose and insulin levels in humans. Our findings underscore a role of the feimin–MERTK signalling axis in glucose homeostasis, providing valuable insights into potential therapeutic avenues for diabetes.</p>

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A feeding-induced myokine modulates glucose homeostasis

  • 期刊论文

  • 发表日期：

    2025年1月2日

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  • Xiaoliu Shi,
  • Xiao Hu,
  • Xinlei Fang,
  • Liangjie Jia,
  • Fangchao Wei,
  • Ying Peng,
  • Menghao Liu,
  • Aibo Gao,
  • Ke Zhao,
  • Fengyi Chen,
  • Xiaoli Hu,
  • Jie Hong,
  • Guang Ning,
  • Yongfeng Song,
  • Jiqiu Wang,
  • Yiguo Wang

摘要

Maintaining blood glucose homeostasis during fasting and feeding is crucial for the prevention of dysregulation that can lead to either hypo- or hyperglycaemia. Here we identified feimin, encoded by a gene with a previously unknown function (B230219D22Rik in mice, C5orf24 in humans), as a key modulator of glucose homeostasis. Feimin is secreted from skeletal muscle during feeding and binds to its receptor, receptor protein tyrosine kinase Mer (MERTK), promoting glucose uptake and inhibiting glucose production by activation of AKT. Administration of feimin and insulin synergistically improves blood glucose homeostasis in both normal and diabetic mice. Notably, a specific single nucleotide polymorphism (rs7604639, G>A) within the MERTK gene, causing an amino acid substitution (R466K) within the feimin–MERTK binding region, leads to reduced association with feimin and elevated postprandial blood glucose and insulin levels in humans. Our findings underscore a role of the feimin–MERTK signalling axis in glucose homeostasis, providing valuable insights into potential therapeutic avenues for diabetes.