Signalling to glucose transport in skeletal muscle during exercise

• Published in: Acta physiologica Scandinavica 2003-08, Vol.178 (4), p.329-335
• Main Authors: Richter, E. A., Nielsen, J. N., Jørgensen, S. B., Frøsig, C., Wojtaszewski, J. F. P.
• Format: Article
• Language: English
• Subjects: AMP-activated protein kinase; AMP-Activated Protein Kinases; Animals; Biological and medical sciences; Biological Transport - physiology; Calcium - metabolism; contraction; Exercise - physiology; Feedback, Physiological - physiology; Fundamental and applied biological sciences. Psychology; Glucose - metabolism; Humans; Mitogen-Activated Protein Kinases - metabolism; Multienzyme Complexes - metabolism; Muscle, Skeletal - metabolism; p38 MAP-kinase; protein kinase C; Protein-Serine-Threonine Kinases - metabolism; Signal Transduction - physiology; Striated muscle. Tendons; Vertebrates: osteoarticular system, musculoskeletal system
• ISSN: 0001-6772; 1365-201X
• DOI: 10.1046/j.1365-201X.2003.01153.x

Exercise‐induced glucose uptake in skeletal muscle is mediated by an insulin‐independent mechanism. Although the signalling events that increase glucose transport in response to muscle contraction are not fully elucidated, the aim of the present review is to briefly present the current understanding of the molecular signalling mechanisms involved. Glucose uptake may be regulated by Ca++‐sensitive contraction‐related mechanisms possibly involving protein kinase C, and by mechanisms that reflect the metabolic status of the muscle and may involve the AMP‐activated protein kinase. Furthermore the p38 mitogen activated protein kinase may be involved. Still, the picture is incomplete and a substantial part of the exercise/contraction‐induced signalling mechanism to glucose transport remains unknown.