Role of glucose transport in glycogen supercompensation in
reweighted rat skeletal muscle.
Henriksen, Erik J., Craig S. Stump, Thanh-Hang T. Trinh, and Sean D.
Beaty.
Muscle Metabolism Laboratory, Department of Physiology, University
of Arizona College of Medicine, Tucson, AZ 85721-0093
APStracts 2:0554A, 1995.
Hindlimb weight-bearing following a 3-day period of hindlimb
suspension (reweighting) of juvenile rats results in a marked,
transient elevation in soleus glycogen concentration, which cannot be
explained based on the activities of glycogen synthase and
phosphorylase. We have hypothesized that enhanced glucose transport
activity could underlie this response. We directly tested this
hypothesis by assessing the response of insulin-dependent and
insulin-independent glucose transport activity (in vitro 2
-deoxyglucose uptake), as well as glucose transporter (GLUT-4) protein
levels, during a 48 h reweighting period. Following a net glycogen
loss (from 29 +/- 2 nmol/mg muscle to 16 +/- 1, P<0.05) during
the first 2 h of reweighting, glycogen accumulated at an average rate
of 1.4 nmol/mg/hr up to 18 h, reaching an apex of 38 +/- 1. During
this same reweighting period, insulin-independent, but not insulin
-dependent, glucose transport activity was significantly enhanced
(P<0.05 vs. weight-bearing control) and was associated with an
elevated level of GLUT-4 protein and the specific activity of total
hexokinase. The specific activity of citrate synthase was also
increased. By 24 h of reweighting, although insulin-independent
glucose transport activity and GLUT-4 protein remained elevated,
glycogen accumulation had ceased, likely due to our previous
observation of enhanced phosphorylase activity at this time point.
These results are consistent with the interpretation that the
glycogen supercompensation seen during reweighting of the rat soleus
may be regulated in part by an enhanced glucose flux arising from an
increase in insulin-independent glucose transport activity and
hexokinase activity.
Received 27 September 1995; accepted in final form 5 December
1995.
APS Manuscript Number A1044-5.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 23 December 95