DIFFERENTIAL EFFECT OF MATURATION ON INSULIN-STIMULATED VS CONTRACTION-STIMULATED GLUCOSE-TRANSPORT IN ZUCKER RATS

Citation
Pl. Dolan et al., DIFFERENTIAL EFFECT OF MATURATION ON INSULIN-STIMULATED VS CONTRACTION-STIMULATED GLUCOSE-TRANSPORT IN ZUCKER RATS, American journal of physiology: endocrinology and metabolism, 31(6), 1995, pp. 1154-1160
Citations number
22
Categorie Soggetti
Physiology
ISSN journal
01931849
Volume
31
Issue
6
Year of publication
1995
Pages
1154 - 1160
Database
ISI
SICI code
0193-1849(1995)31:6<1154:DEOMOI>2.0.ZU;2-W
Abstract
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 contract ion-stimulated pathway for glucose transport was similarly affected, g lucose transport rates were measured in insulin- and electrically stim ulated skeletal muscle during hindlimb perfusion of 10- and 29-wk-old lean and obese male Zucker rats. Glucose transporter (GLUT-4) protein was also measured. Insulin-stimulated glucose transport rates were sig nificantly decreased (36-56%) in 29-wk compared with 10-wk-old lean ra ts. There was no maturation-related decrease in GLUT-4. Insulin-mediat ed 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- than 29-wk-old animals. Maturation had no effect on contraction-stimulated glucose transport rates in ei ther lean or obese animals. The combined effect of maximal insulin plu s contraction was not altered with maturity in lean animals but was si gnificantly increased in 29- compared with 10-wk-old obese rats. Absen ce of a change in GLUT-4 content together with uncompromised contracti on-stimulated glucose transport suggests that the maturation-induced d ecrease in insulin-stimulated glucose transport in lean rats is due to a defect in the insulin signaling pathway.