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<p>CD59 is known as a membrane-bound regulator of the complement system that prevents the formation of the membrane attack complex on host cells. Here we report the metabolic consequences of CD59a knockout (KO) in mice fed a high-fat diet (HFD). Mice lacking CD59a were protected from the development of insulin resistance, glucose intolerance, hyperinsulinemia, obesity, and fatty liver. Mutants fed an HFD had elevated adiponectin levels and reduced leptin levels in plasma. Data from metabolic cages suggested decreased appetite and an increase in voluntary wheel activity in mutants. Liver transcriptome analysis showed a marked decrease of inflammatory and fibrotic pathways in CD59a KO mice on an HFD, and plasma and liver metabolomics were remarkably similar, indicating close correspondence between systemic and hepatic metabolic profiles. In conclusion, we uncover a noncanonical role of CD59a in the development of diet-induced insulin resistance, hyperinsulinemia, glucose intolerance, and obesity.</p>

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CD59 drives diet-induced obesity and glucose intolerance, insulin resistance, and metabolic dysfunction-associated steatotic liver disease

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月17日

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  • Marian Zeibak,
  • Netanel Karbian,
  • Yael Riahi,
  • Saja Baraghithy,
  • Labiba Ahmad,
  • Adi Tabib,
  • Ifat Abromovitz,
  • Bella Agranovitz,
  • Hadar Benyamini,
  • Eyal Gottlieb,
  • Joseph Tam,
  • Yuval Dor,
  • Gil Leibowitz,
  • Dror Mevorach

摘要

CD59 is known as a membrane-bound regulator of the complement system that prevents the formation of the membrane attack complex on host cells. Here we report the metabolic consequences of CD59a knockout (KO) in mice fed a high-fat diet (HFD). Mice lacking CD59a were protected from the development of insulin resistance, glucose intolerance, hyperinsulinemia, obesity, and fatty liver. Mutants fed an HFD had elevated adiponectin levels and reduced leptin levels in plasma. Data from metabolic cages suggested decreased appetite and an increase in voluntary wheel activity in mutants. Liver transcriptome analysis showed a marked decrease of inflammatory and fibrotic pathways in CD59a KO mice on an HFD, and plasma and liver metabolomics were remarkably similar, indicating close correspondence between systemic and hepatic metabolic profiles. In conclusion, we uncover a noncanonical role of CD59a in the development of diet-induced insulin resistance, hyperinsulinemia, glucose intolerance, and obesity.