ArticleMolecular metabolism2014
Contraction-stimulated glucose transport in muscle is controlled by AMPK and mechanical stress but not sarcoplasmatic reticulum Ca(2+) release.
Article in Molecular metabolism, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 84 citations in OpenAlex.
- Preventing Metabolic Syndrome in Adolescents Through Exercise.Advances in experimental medicine and biology · 2026Review
- Mechanomedicine for Addressing Skeletal Muscle Insulin Resistance.Endocrine reviews · 2025Review
- Insulin- and exercise-induced phosphoproteomics of human skeletal muscle identify REPS1 as a regulator of muscle glucose uptake.Cell reports. Medicine · 2025Article
- Pantothenate kinase 4 controls skeletal muscle substrate metabolism.Nature communications · 2025Article
- Intrinsic Skeletal Muscle Function and Contraction-Stimulated Glucose Uptake Do Not Vary by Time-of-Day in Mice.Function (Oxford, England) · 2024Article
- How Can Promoting Skeletal Muscle Health and Exercise in Children and Adolescents Prevent Insulin Resistance and Type 2 Diabetes?Life (Basel, Switzerland) · 2024Review
- Salicylate induces epithelial actin reorganization via activation of the AMP-activated protein kinase and promotes wound healing and contraction in mice.Scientific reports · 2024Article
- Effect of Exercise Conditioning on Countering the Effects of Obesity and Insulin Resistance in Horses-A Review.Animals : an open access journal from MDPI · 2024Review
- Acute Low Force Electrically Induced Exercise Modulates Post Prandial Glycemic Markers in People with Spinal Cord Injury.Journal of functional morphology and kinesiology · 2022Article
- Involvement of the extracellular matrix and integrin signalling proteins in skeletal muscle glucose uptake.The Journal of physiology · 2022Review
- Influences on PET Quantification and Interpretation.Diagnostics (Basel, Switzerland) · 2022Review
- Measurement of skeletal muscle glucose uptake in mice in response to acute treadmill running.Journal of biological methods · 2022Article
- Exercise increases phosphorylation of the putative mTORC2 activity readout NDRG1 in human skeletal muscle.American journal of physiology. Endocrinology and metabolism · 2022Article
- A Critical Review of the Biochemical Mechanisms and Epigenetic Modifications in HIV- and Antiretroviral-Induced Metabolic Syndrome.International journal of molecular sciences · 2021Review
- Modified UCN2 peptide treatment improves skeletal muscle mass and function in mouse models of obesity-induced insulin resistance.Journal of cachexia, sarcopenia and muscle · 2021Article
- Is GLUT4 translocation the answer to exercise-stimulated muscle glucose uptake?American journal of physiology. Endocrinology and metabolism · 2021Article
- Tmod3 Phosphorylation Mediates AMPK-Dependent GLUT4 Plasma Membrane Insertion in Myoblasts.Frontiers in endocrinology · 2021Article
- Pathophysiology of exercise-induced muscle damage and its structural, functional, metabolic, and clinical consequences.Physiological research · 2020Review
- Role of Skeletal Muscle in Insulin Resistance and Glucose Uptake.Comprehensive Physiology · 2020Review
- The ULK1/2 and AMPK Inhibitor SBI-0206965 Blocks AICAR and Insulin-Stimulated Glucose Transport.International journal of molecular sciences · 2020Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Understanding how muscle contraction orchestrates insulin-independent muscle glucose transport may enable development of hyperglycemia-treating drugs. The prevailing concept implicates Ca(2+) as a key feed forward regulator of glucose transport with secondary fine-tuning by metabolic feedback signals through proteins such as AMPK. Here, we demonstrate in incubated mouse muscle that Ca(2+) release is neither sufficient nor strictly necessary to increase glucose transport. Rather, the glucose transport response is associated with metabolic feedback signals through AMPK, and mechanical stress-activated signals. Furthermore, artificial stimulation of AMPK combined with passive stretch of muscle is additive and sufficient to elicit the full contraction glucose transport response. These results suggest that ATP-turnover and mechanical stress feedback are sufficient to fully increase glucose transport during muscle contraction, and call for a major reconsideration of the established Ca(2+) centric paradigm.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.