Journal of Applied Physiology Ad Instruments
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

J Appl Physiol 102: 1671-1676, 2007. First published November 2, 2006; doi:10.1152/japplphysiol.01066.2006
8750-7587/07 $8.00
This Article
Right arrow Full Text Free
Right arrow Full Text (PDF) Free
Right arrow All Versions of this Article:
102/4/1671    most recent
01066.2006v1
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (7)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Katz, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Katz, A.

INVITED REVIEW

HIGHLIGHTED TOPIC
Free Radical Biology in Skeletal Muscle

Modulation of glucose transport in skeletal muscle by reactive oxygen species

Abram Katz

Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden

Glucose transport is an essential physiological process that is characteristic of all eukaryotic cells, including skeletal muscle. In skeletal muscle, glucose transport is mediated by the GLUT-4 protein under conditions of increased carbohydrate utilization. The three major physiological stimuli of glucose transport in muscle are insulin, exercise/contraction, and hypoxia. Here, the role of reactive oxygen species (ROS) in modulating glucose transport in skeletal muscle is reviewed. Convincing evidence for ROS involvement in insulin- and hypoxia-mediated transport in muscle is lacking. Recent experiments, based on pharmacological and genetic approaches, support a role for ROS in contraction-mediated glucose transport. During contraction, endogenously produced ROS appear to mediate their effects on glucose transport via AMP-activated protein kinase.

exercise; adenosine 5'-monophosphate-activated protein kinase


Address for reprint requests and other correspondence: A. Katz, Dept. of Physiology and Pharmacology, Karolinska Institutet, 171 77 Stockholm, Sweden (e-mail: abram.katz{at}ki.se)




This article has been cited by other articles:


Home page
 Am. J. Physiol. Endocrinol. Metab.Home page
D. R. Blair, K. Funai, G. G. Schweitzer, and G. D. Cartee
A myosin II ATPase inhibitor reduces force production, glucose transport, and phosphorylation of AMPK and TBC1D1 in electrically stimulated rat skeletal muscle
Am J Physiol Endocrinol Metab, May 1, 2009; 296(5): E993 - E1002.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Endocrinol. Metab.Home page
A. Natalicchio, F. De Stefano, S. Perrini, L. Laviola, A. Cignarelli, C. Caccioppoli, A. Quagliara, M. Melchiorre, A. Leonardini, A. Conserva, et al.
Involvement of the p66Shc protein in glucose transport regulation in skeletal muscle myoblasts
Am J Physiol Endocrinol Metab, February 1, 2009; 296(2): E228 - E237.
[Abstract] [Full Text] [PDF]

Home page
 Physiol. Rev.Home page
N. Bashan, J. Kovsan, I. Kachko, H. Ovadia, and A. Rudich
Positive and Negative Regulation of Insulin Signaling by Reactive Oxygen and Nitrogen Species
Physiol Rev, January 1, 2009; 89(1): 27 - 71.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
Y. Lecarpentier
Physiological role of free radicals in skeletal muscles
J Appl Physiol, December 1, 2007; 103(6): 1917 - 1918.
[Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
M. B. Reid
Editorial
J Appl Physiol, April 1, 2007; 102(4): 1299 - 1300.
[Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2007 by the American Physiological Society.