Inhibition of contraction-stimulated AMP-activated protein kinase inhibits contraction-stimulated increases in PAS-TBC1D1 and glucose transport without altering PAS-AS160 in rat skeletal muscle.
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Emerging role of the brain in the homeostatic regulation of energy and glucose metabolismSkeletal muscle nitric oxide signaling and exercise: a focus on glucose metabolismMetabolic benefits of resistance training and fast glycolytic skeletal muscle.Contraction regulates site-specific phosphorylation of TBC1D1 in skeletal muscleGenetic disruption of AMPK signaling abolishes both contraction- and insulin-stimulated TBC1D1 phosphorylation and 14-3-3 binding in mouse skeletal muscleInsulin-stimulated phosphorylation of the Rab GTPase-activating protein TBC1D1 regulates GLUT4 translocationExercise and type 2 diabetes: molecular mechanisms regulating glucose uptake in skeletal muscle.Muscle lipogenesis balances insulin sensitivity and strength through calcium signaling.Exercise and Glycemic Control: Focus on Redox Homeostasis and Redox-Sensitive Protein Signaling.In vivo exercise followed by in vitro contraction additively elevates subsequent insulin-stimulated glucose transport by rat skeletal muscle.TBC1D1 regulates insulin- and contraction-induced glucose transport in mouse skeletal muscle.Leptin reduces the expression and increases the phosphorylation of the negative regulators of GLUT4 traffic TBC1D1 and TBC1D4 in muscle of ob/ob mice.Deficiency in AMP-activated protein kinase exaggerates high fat diet-induced cardiac hypertrophy and contractile dysfunctionRoles of TBC1D1 and TBC1D4 in insulin- and exercise-stimulated glucose transport of skeletal muscleFiber type effects on contraction-stimulated glucose uptake and GLUT4 abundance in single fibers from rat skeletal muscleNaturally occurring compensated insulin resistance selectively alters glucose transporters in visceral and subcutaneous adipose tissues without change in AS160 activationMechanisms for independent and combined effects of calorie restriction and acute exercise on insulin-stimulated glucose uptake by skeletal muscle of old rats.17-β estradiol attenuates ovariectomy-induced changes in cardiomyocyte contractile function via activation of AMP-activated protein kinase.Reduced efficiency of sarcolipin-dependent respiration in myocytes from humans with severe obesity.Skeletal Muscle Phospholipid Metabolism Regulates Insulin Sensitivity and Contractile Function.AMPK and Exercise: Glucose Uptake and Insulin Sensitivity.Immobilization rapidly induces muscle insulin resistance together with the activation of MAPKs (JNK and p38) and impairment of AS160 phosphorylationA myosin II ATPase inhibitor reduces force production, glucose transport, and phosphorylation of AMPK and TBC1D1 in electrically stimulated rat skeletal muscleIncreased AS160 phosphorylation, but not TBC1D1 phosphorylation, with increased postexercise insulin sensitivity in rat skeletal muscle.IGF-1 deficiency resists cardiac hypertrophy and myocardial contractile dysfunction: role of microRNA-1 and microRNA-133a.Exercise and insulin: Convergence or divergence at AS160 and TBC1D1?Central insulin and leptin-mediated autonomic control of glucose homeostasis.Adenosine Monophosphate-Activated Protein Kinase (AMPK) as a New Target for Antidiabetic Drugs: A Review on Metabolic, Pharmacological and Chemical Considerations.Targeting the liver kinase B1/AMP-activated protein kinase pathway as a therapeutic strategy for hematological malignancies.Role of AMP-Activated Protein Kinase for Regulating Post-exercise Insulin Sensitivity.Phosphatidylinositol 3-phosphate 5-kinase (PIKfyve) is an AMPK target participating in contraction-stimulated glucose uptake in skeletal muscle.Caffeine and contraction synergistically stimulate 5'-AMP-activated protein kinase and insulin-independent glucose transport in rat skeletal muscle.Thr649Ala-AS160 knock-in mutation does not impair contraction/AICAR-induced glucose transport in mouse muscleIdentification and Association of SNPs in TBC1D1 Gene with Growth Traits in Two Rabbit Breeds.Restoring AS160 phosphorylation rescues skeletal muscle insulin resistance and fatty acid oxidation while not reducing intramuscular lipids.Exercise-induced TBC1D1 Ser237 phosphorylation and 14-3-3 protein binding capacity in human skeletal muscle.N-Acetylcysteine infusion does not affect glucose disposal during prolonged moderate-intensity exercise in humans.Increased postexercise insulin sensitivity is accompanied by increased AS160 phosphorylation in slow-twitch soleus muscle.Elevation of muscle temperature stimulates muscle glucose uptake in vivo and in vitro.The Beneficial Effect of Anthocyanidin-Rich Vitis vinifera L. Grape Skin Extract on Metabolic Changes Induced by High-Fat Diet in Mice Involves Antiinflammatory and Antioxidant Actions.
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Inhibition of contraction-stimulated AMP-activated protein kinase inhibits contraction-stimulated increases in PAS-TBC1D1 and glucose transport without altering PAS-AS160 in rat skeletal muscle.
description
article científic
@ca
article scientifique
@fr
articolo scientifico
@it
artigo científico
@pt
bilimsel makale
@tr
scientific article published on 10 February 2009
@en
vedecký článok
@sk
vetenskaplig artikel
@sv
videnskabelig artikel
@da
vědecký článek
@cs
name
Inhibition of contraction-stim ...... -AS160 in rat skeletal muscle.
@en
Inhibition of contraction-stim ...... -AS160 in rat skeletal muscle.
@nl
type
label
Inhibition of contraction-stim ...... -AS160 in rat skeletal muscle.
@en
Inhibition of contraction-stim ...... -AS160 in rat skeletal muscle.
@nl
prefLabel
Inhibition of contraction-stim ...... -AS160 in rat skeletal muscle.
@en
Inhibition of contraction-stim ...... -AS160 in rat skeletal muscle.
@nl
P2860
P356
P1433
P1476
Inhibition of contraction-stim ...... -AS160 in rat skeletal muscle.
@en
P2093
Gregory D Cartee
Katsuhiko Funai
P2860
P304
P356
10.2337/DB08-1477
P407
P577
2009-02-10T00:00:00Z