UNASSIGNED: Acute exercise increases @entity413 uptake in skeletal muscle by an insulin-independent mechanism. In the period after exercise insulin sensitivity to increase @entity413 uptake is enhanced. The molecular mechanisms underpinning this phenomenon are poorly understood, but appear to involve an increased cell surface abundance of @entity3240 . While increased proximal insulin signaling does not seem to mediate this effect, elevated phosphorylation of @entity54807 , a downstream target of both insulin ( @entity1994 ) and exercise (AMPK) signaling, appears to play a role. The main purpose of this study was to determine whether AMPK activation increases skeletal muscle insulin sensitivity. We found that prior AICAR stimulation of wild-type @entity19 muscle @entity1720 to stimulate @entity413 uptake. However, this was not observed in @entity19 with reduced or ablated AMPK activity in skeletal muscle. Furthermore, prior AICAR stimulation enhanced insulin-stimulated phosphorylation of @entity54807 at Thr(649) and Ser(711) in wild-type muscle only. These phosphorylation events were positively correlated with @entity413 uptake. Our results provide evidence to support that AMPK is sufficient to increase skeletal muscle insulin sensitivity. Moreover, @entity54807 phosphorylation may facilitate the effect of prior AMPK activation to enhance @entity413 uptake in response to insulin.

Prior AICAR stimulation @entity1720 in XXXX skeletal muscle in an AMPK-dependent manner.

@entity19 :: ('10090', 'Species') :: ['mice', 'mouse'] @entity54807 :: ('210789(Tax:10090)', 'Gene') :: ['TBC1D4'] @entity3240 :: ('20528(Tax:10090)', 'Gene') :: ['GLUT4'] @entity1994 :: ('11651(Tax:10090)', 'Gene') :: ['Akt'] @entity1720 :: ('MESH:D007333', 'Disease') :: ['increases insulin sensitivity'] @entity413 :: ('MESH:D005947', 'Chemical') :: ['glucose']
@entity19 :: (10090,Species) :: ['mouse']
