Differential effect of maturation on insulin- versus contraction-stimulated
glucose transport in zucker rats..
Dolan, P. L., S. G. Boyd, and G. L. Dohm.
Dept. of Biochemistry, East Carolina University School of Medicine,
Greenville, North Carolina 27858.
APStracts 2:0007E, 1995.
Insulin-stimulated glucose transport has been shown to decline during
maturation in lean rats. To determine whether this maturation-induced
decrease occurred in the muscle of obese rats and whether the contraction
-stimulated pathway for glucose transport was similarly affected, glucose
transport rates were measured in insulin- and electrically-stimulated
skeletal muscle during hindlimb perfusion of 10- and 29-wk-old lean and obese
male Zucker rats. Glucose transporter (GLUT4) protein was also measured.
Insulin-stimulated glucose transport rates were significantly decreased (36%
- 56 %) in 29-wk compared to 10-wk-old lean rats. There was no maturation
-related decrease in GLUT4. Insulin-mediated glucose transport was unaltered
by maturation in skeletal muscle of obese rats. Differential effects of
maturation on lean and obese rats caused the effect of obesity on maximally
insulin-stimulated glucose transport to be much greater in 10-wk than 29-wk
-old animals. Maturation had no effect on contraction-stimulated glucose
transport rates in either lean or obese animals. The combined effect of
maximal insulin plus contraction was not altered with maturity in lean
animals, but was significantly increased in the 29-wk compared to 10-wk-old
obese rats. Absence of a change in GLUT4 content together with uncompromised
contraction-stimulated glucose transport suggests that the maturation-induced
decrease in insulin-stimulated glucose transport in lean rats is due to a
defect in the insulin signalling pathway.
Received 22 July 1994; accepted in final form 13 January 1995.
APS Manuscript Number E285-4.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 25 February 1995.