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Dadun > Depósito Académico > Facultad de Farmacia > Departamento de Ciencias de la Alimentación, Fisiología y Toxicología > DA - Farmacia - CAFT - Artículos de revista >

Eicosapentaenoic acid stimulates AMP-activated protein kinase and increases visfatin secretion in cultured murine adipocytes
Autor(es) : Lorente-Cebrian, S. (Silvia)
Bustos, M. (Matilde)
Marti, A. (Amelia)
Martinez, J.A. (Jose Alfredo)
Moreno-Aliaga, M.J. (María Jesús)
Palabras clave : AMP-activada proteína kinasa (AMPK)
Tejido adiposo
Visfatin
Fecha incorporación: 2009
Editorial : Portland Press
Versión del editor: http://www.clinsci.org/cs/117/cs1170243.htm
ISSN: 1470-8736
Cita: Lorente-Cebrian S, Bustos M, Marti A, Martinez JA, Moreno-Aliaga MJ. Eicosapentaenoic acid stimulates AMP-activated protein kinase and increases visfatin secretion in cultured murine adipocytes. Clin.Sci.(Lond) 2009 Aug 14;117(6):243-249.
Resumen
Visfatin is an adipokine highly expressed in visceral AT (adipose tissue) of humans and rodents, the production of which seems to be dysregulated in excessive fat accumulation and conditions of insulin resistance. EPA (eicosapentaenoic acid), an n−3 PUFA (polyunsaturated fatty acid), has been demonstrated to exert beneficial effects in obesity and insulin resistance conditions, which have been further linked to its reported ability to modulate adipokine production by adipocytes. TNF-α (tumour necrosis factor-α) is a pro-inflammatory cytokine whose production is increased in obesity and is involved in the development of insulin resistance. Control of adipokine production by some insulin-sensitizing compounds has been associated with the stimulation of AMPK (AMP-activated protein kinase). The aim of the present study was to examine in vitro the effects of EPA on visfatin production and the potential involvement of AMPK both in the absence or presence of TNF-α. Treatment with the pro-inflammatory cytokine TNF-α (1 ng/ml) did not modify visfatin gene expression and protein secretion in primary cultured rat adipocytes. However, treatment of these primary adipocytes with EPA (200 μmol/l) for 24 h significantly increased visfatin secretion (P<0.001) and mRNA gene expression (P<0.05). Moreover, the stimulatory effect of EPA on visfatin secretion was prevented by treatment with the AMPK inhibitor Compound C, but not with the PI3K (phosphoinositide 3-kinase) inhibitor LY294002. Similar results were observed in 3T3-L1 adipocytes. Moreover, EPA strongly stimulated AMPK phosphorylation alone or in combination with TNF-α in 3T3-L1 adipocytes and pre-adipocytes. The results of the present study suggest that the stimulatory action of EPA on visfatin production involves AMPK activation in adipocytes.
Enlace permanente: http://hdl.handle.net/10171/13364
Aparece en las colecciones: DA - Farmacia - CAFT - Línea Especial de Nutrición
DA - Farmacia - CAFT - Artículos de revista

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