A role for AMP-activated protein kinase in contraction- and hypoxia-regulated glucose transport in skeletal muscle.

By J. Mu, J. Brozinick, O. Valladares, Maja Bucan, M. Birnbaum. Molecules and Cells, 2001

994 citations recorded by the source corpus.

Subfields: Molecular Biology, Physiology, Surgery

View Paper: https://www.semanticscholar.org/paper/d5d3b29dfba1184d416eda3108613e5b92ba5cb9

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Citations in the corpus

Metformin increases AMP-activated protein kinase activity in skeletal muscle of subjects with type 2 diabetes. (2002, background): “AICAR cannot stimulate muscle glucose uptake in mice carrying a kinase-dead AMPK mutant in muscle (19).”
AMP‐activated protein kinase: the energy charge hypothesis revisited (2001, background): “Using transgenic mice in which AMPK activity was almost abolished in muscle by expression of a dominant negative mutant, Birnbaum's group have recently shown that the effect of contraction on muscle glucose uptake was partly eliminated, while the effect of hypoxia was completely eliminated.((31)) Th”
Muscle‐derived interleukin‐6: mechanisms for activation and possible biological roles (2002, background): “(102) recently demonstrated that although contraction-induced glucose uptake was reduced in an AMPK null transgenic mouse it was only partially reduced.”
Physical activity/exercise and type 2 diabetes. (2004, background): “Such a role for this enzyme is supported by the demonstration that pharmacological activation of AMP kinase stimulates GLUT4 translocation (38) and glucose uptake (36,39,40) and is linked to other changes in enzyme activities (35,41) and gene transcription (42,43) associated with exercise.”
The antidiabetic drug metformin activates the AMP-activated protein kinase cascade via an adenine nucleotide-independent mechanism. (2002, background): “The AMPK cascade is activated by exercise (9), and studies with transgenic mice expressing a dominant-negative mutant in skeletal muscle suggest that it is wholly responsible for the effects of hypoxia and partly responsible for the effects of contraction on muscle glucose uptake (10).”
The Pleiotropic Actions of Adiponectin are Initiated via Receptor-Mediated Activation of Ceramidase Activity (2010, methodology): “Mouse tissues were processed and western blots were developed as previously describe”
Fiber types in mammalian skeletal muscles. (2011, background): “Mice expressing a dominant negative form of AMPK are intolerant to exercise (551), and the same is true for mice with muscle-specific LKB1 deficiency, which causes lower levels of cytochrome c and PGC-1 protein expression in the red region of the quadriceps (793).”
Interdependence of AMPK and SIRT1 for metabolic adaptation to fasting and exercise in skeletal muscle (2010, background): “…several models of AMPK deficiency display decreased basal mitochondrial gene expression (Jorgensen et al., 2005), lower voluntary exercise activity (Mu et al., 2001), and lower exercise tolerance (Fujii et al., 2007), defective AMPK does not robustly affect exercise-induced gene expression (Barnes…”