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Mecanismos moleculares por los cuales los ácidos grasos podrían influir en la captación de glucosa
Molecular mechanisms by which free fatty acids might interfere with periferic insuline action
Palabras clave:
ácidos grasos, diabetes mellitus, obesidad, insulina, glucosa, hiperglucemia, xilulosa, glucólisis. (es)fatty acids, diabetes mellitus, obesity, insulin, glucose, hyperglycemia, xylulose, glycolysis. (en)
Esta revisión tiene el propósito de actualizar el probable mecanismo molecular que ejercen los ácidos grasos en las células que captan glucosa, bajo el estimulo de la insulina y su posible implicación en la diabetes mellitus tipo 2 en la que suelen asociarse resistencia a la insulina, obesidad y síndrome metabólico.
Entre los mecanismos moleculares por los cuales un aumento de los ácidos grasos libres podría producir resistencia a la insulina, se encuentra la disminución de los niveles de xilulosa 5-fosfato que bloquea la glucólisis por inhibición de la fosfofructocinasa, ello conduce a un aumento de los productos finales en la vía de las hexosaminas y a la activación de la proteincinasa C, un conocido activador de inhibidor de la cinasa Kappa Beta que inhibe la fosforilación del receptor del sustrato de insulina en tirosina, bloqueando los transportadores de glucosa. Existen investigaciones que sugieren que los ácidos grasos libres están implicados en la insulino-resistencia pero el mecanismo bioquímico no esta dilucidado del todo, pues no hay un mecanismo integral que los relacione o interconecte para concluir determinantemente cómo los altos niveles de ácidos grasos libres inducen la resistencia a la insulina.
Previous research suggests that free fatty acids are implicated in insulin resistance, but the molecular mechanism for it isn't completely elucidated, given the lack of an integrated hypothesis relating all of the proposed mechanisms. At the present time, the causes of insulin resistance, obesity and metabolic syndrome, a common feature in patients with diabetes mellitus are matter of intense study.
Among several molecular mechanisms by which the increase in free fatty acids could raise insulin resistance is decrease in xylulose-5-phosphate that leads to an inhibition of phosphofructokinase-2, and consequently to a blockade in glycol sis with a subsequent increase in the final products of the hexosamine pathway and activation of PKC has been proposed as well as known activator of IKKB that inhibits tyrosine phosphorilation of IRS, hindering glucose transport.
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Derechos de autor 2005 Revista de la Facultad de Medicina
Esta obra está bajo una licencia internacional Creative Commons Atribución 4.0.
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