HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 291/6/E1258    most recent 00273.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via ISI Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Geiger, P. C. Articles by Holloszy, J. O. Search for Related Content PubMed PubMed Citation Articles by Geiger, P. C. Articles by Holloszy, J. O.

How muscle insulin sensitivity is regulated: testing of a hypothesis

Department of Medicine, Washington University School of Medicine, St. Louis, Missouri

Submitted 7 June 2006 ; accepted in final form 7 July 2006

Muscle contractions induce an increase in glucose transport. The acute effect of muscle contractions on glucose transport is independent of insulin and reverses rapidly after cessation of exercise. As the acute increase in glucose transport reverses, a marked increase in the sensitivity of muscle to insulin occurs. The mechanism for this phenomenon is unknown. We hypothesize that an increase in insulin sensitivity is a general phenomenon that occurs during reversal of an increase in cell surface GLUT4 induced by any stimulus, not just exercise. To test this hypothesis, epitrochlearis, rat soleus, and flexor digitorum brevis muscles were incubated for 30 min with a maximally effective insulin concentration (1.0 mU/ml). Muscles were allowed to recover for 3 h in the absence of insulin. Muscles were then exposed to 60 µU/ml insulin for 30 min followed by measurement of glucose transport. Preincubation with 1.0 mU/ml insulin resulted in an 2-fold greater increase in glucose transport 3.5 h later in response to 60 µU/ml insulin than that which occurred in control muscles treated with 60 µU/ml insulin. Pretreatment of muscles with combined maximal insulin and exercise stimuli greatly amplified the increase in insulin sensitivity. The increases in glucose transport were paralleled by increases in cell surface GLUT4. We conclude that stimulation of glucose transport by any agent is followed by an increase in sensitivity of glucose transport to activation that is mediated by translocation of more GLUT4 to the cell surface.

hypoxia; exercise; glucose transport; glucose transporter 4