Mifepristone enhances insulin-stimulated Akt phosphorylation and glucose uptake in skeletal muscle cells

Izela Bernal-Sore, Mario Navarro-Marquez, César Osorio-Fuentealba, Francisco Díaz-Castro, Andrea del Campo, Camila Donoso-Barraza, Omar Porras, Sergio Lavandero, Rodrigo Troncoso

Research output: Contribution to journalArticlepeer-review

5 Citations (Scopus)


Mifepristone is the only FDA-approved drug for glycaemia control in patients with Cushing's syndrome and type 2 diabetes. Mifepristone also has beneficial effects in animal models of diabetes and patients with antipsychotic treatment-induced obesity. However, the mechanisms through which Mifepristone produces its beneficial effects are not completely elucidated. Purpose To determine the effects of mifepristone on insulin-stimulated glucose uptake on a model of L6 rat-derived skeletal muscle cells. Results Mifepristone enhanced insulin-dependent glucose uptake, GLUT4 translocation to the plasma membrane and Akt Ser 473 phosphorylation in L6 myotubes. In addition, mifepristone reduced oxygen consumption and ATP levels and increased AMPK Thr 172 phosphorylation. The knockdown of AMPK prevented the effects of mifepristone on insulin response. Conclusions Mifepristone enhanced insulin-stimulated glucose uptake through a mechanism that involves a decrease in mitochondrial function and AMPK activation in skeletal muscle cells.

Original languageEnglish
Pages (from-to)277-283
Number of pages7
JournalMolecular and Cellular Endocrinology
Publication statusPublished - 5 Feb 2018
Externally publishedYes


  • AMPK
  • Insulin
  • L6 rat cells
  • Mifepristone
  • Mitochondria
  • RU486

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Endocrinology


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