Gene interactions and pathways from curated databases and text-mining
J Clin Endocrinol Metab 2011, PMID: 21508135

Impaired muscle AMPK activation in the metabolic syndrome may attenuate improved insulin action after exercise training.

Layne, Andrew S; Nasrallah, Sami; South, Mark A; Howell, Mary E A; McCurry, Melanie P; Ramsey, Michael W; Stone, Michael H; Stuart, Charles A

BACKGROUND

Strength training induces muscle remodeling and may improve insulin responsiveness.

OBJECTIVE

This study will quantify the impact of resistance training on insulin sensitivity in subjects with the metabolic syndrome and correlate this with activation of intramuscular pathways mediating mitochondrial biogenesis and muscle fiber hypertrophy.

METHODS

Ten subjects with the metabolic syndrome (MS) and nine sedentary controls underwent 8 wk of supervised resistance exercise training with pre- and posttraining anthropometric and muscle biochemical assessments.

METHODS

Resistance exercise training took place in a sports laboratory on a college campus.

METHODS

Pre- and posttraining insulin responsiveness was quantified using a euglycemic clamp. Changes in expression of muscle 5-AMP-activated protein kinase (AMPK) and mammalian target of rapamycin (mTOR) pathways were quantified using immunoblots.

RESULTS

Strength and stamina increased in both groups. Insulin sensitivity increased in controls (steady-state glucose infusion rate = 7.0 ± 2.0 mg/kg · min pretraining training vs. 8.7 ± 3.1 mg/kg · min posttraining; P < 0.01) but did not improve in MS subjects (3.3 ± 1.3 pre vs. 3.1 ± 1.0 post). Muscle glucose transporter 4 increased 67% in controls and 36% in the MS subjects. Control subjects increased muscle phospho-AMPK (43%), peroxisome proliferator-activated receptor γ coactivator 1α (57%), and ATP synthase (60%), more than MS subjects (8, 28, and 21%, respectively). In contrast, muscle phospho-mTOR increased most in the MS group (57 vs. 32%).

CONCLUSIONS

Failure of resistance training to improve insulin responsiveness in MS subjects was coincident with diminished phosphorylation of muscle AMPK, but increased phosphorylation of mTOR, suggesting activation of the mTOR pathway could be involved in inhibition of exercise training-related increases in AMPK and its activation and downstream events.

Diseases/Pathways annotated by Medline MESH: Insulin Resistance, Metabolic Syndrome X
Document information provided by NCBI PubMed

Text Mining Data

mTOR → AMPK: " Failure of resistance training to improve insulin responsiveness in MS subjects was coincident with diminished phosphorylation of muscle AMPK , but increased phosphorylation of mTOR , suggesting activation of the mTOR pathway could be involved in inhibition of exercise training related increases in AMPK and its activation and downstream events "

Manually curated Databases

No curated data.