Mifepristone enhances insulin stimulated Akt phosphorylation and glucose uptake in skeletal muscle cells
Author
dc.contributor.author
Bernal Sore, Izela
Author
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Navarro Márquez, Mario F.
Author
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Osorio Fuentealba, César
Author
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Díaz Castro, Francisco
Author
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Campo, Andrea del
Author
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Donoso Barraza, Camila
Author
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Porras Espinoza, Omar
Author
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Lavandero González, Sergio
Author
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Troncoso Cotal, Rodrigo
Admission date
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2018-07-26T22:43:56Z
Available date
dc.date.available
2018-07-26T22:43:56Z
Publication date
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2018
Cita de ítem
dc.identifier.citation
Molecular and Cellular Endocrinology, 461 (2018): 277-283
es_ES
Identifier
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10.1016/j.mce.2017.09.028
Identifier
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https://repositorio.uchile.cl/handle/2250/150372
Abstract
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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 AMPIC 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 mitochondria! function and AMPK activation in skeletal muscle cells.
es_ES
Patrocinador
dc.description.sponsorship
FONDECYT
1161156
11130424
3140443
11130285
FONDAP grant
15130011
ACT1411