Glycogen overload by postexercise insulin administration abolished the exercise-induced increase in GLUT4 protein

Abstract

To elucidate the role of muscle glycogen storage on regulation of GLUT4 protein expression and whole-body glucose tolerance, muscle glycogen level was manipulated by exercise and insulin administration. Sixty Sprague-Dawley rats were evenly separated into three groups: control (CON), immediately after exercise (EX0), and 16 h after exercise (EX16). Rats from each group were further divided into two groups: saline- and insulin-injected. The 2-day exercise protocol consisted of 2 bouts of 3-h swimming with 45-min rest for each day, which effectively depleted glycogen in both red gastrocnemius (RG) and plantaris muscles. EX0 rats were sacrificed immediately after the last bout of exercise on second day. CON and EX16 rats were intubated with 1 g/kg glucose solution following exercise and recovery for 16 h before muscle tissue collection. Insulin (0.5 microU/kg) or saline was injected daily at the time when glucose was intubated. Insulin injection elevated muscle glycogen levels substantially in both muscles above saline-injected group at CON and EX16. With previous day insulin injection, EX0 preserved greater amount of postexercise glycogen above their saline-injected control. In the saline-injected rats, EX16 significantly increased GLUT4 protein level above CON, concurrent with muscle glycogen supercompensation. Insulin injection for EX16 rats significantly enhanced muscle glycogen level above their saline-injected control, but the increases in muscle GLUT4 protein and whole-body glucose tolerance were attenuated. In conclusion, the new finding of the study was that glycogen overload by postexercise insulin administration significantly abolished the exercise-induced increases in GLUT4 protein and glucose tolerance.

Changes in blood insulin resistance, GLUT4 and AMPK after continuous and interval aerobic training in normal and diabetic rats

“…The increased insulin sensitivity after exercise occurs simultaneously with the accumulation of muscle glycogen stores (Hawley and Lessard, 2008). It is believed that increased muscle glycogen stores after exercise is due to increased GLUT4 (Chou et al, 2005, Tsai et al, 2006 and increased GLUT4 protein displacement from inside the cell to plasma surface (Tsai et al, 2006). The findings of some studies show that exercise (TeixeiraLemos et al, 2011;Eguchi et al, 2013) may impact on AMPK activity and AMPK impact on protein GLUT4 (Teixeira-Lemos et al, 2011;Richter and Hargreaves, 2013).…”

“…The results of researches show that stimulating AMPK increase glucose uptake (Hawley and Lessard 2008). It is believed that the increased muscle glycogen stores after the exercise is due to increased GLUT4 (Chou et al, 2005;Tsai et al, 2006)and increased GLUT4 protein translocation from inside the cell to plasma surface (Tsai et al, 2006). The exercise-stimulation increases in the translocation of GLUT4 to the skeletal muscle cell membrane occur in people who are healthy and in patients with T2DM 8 .…”

The comparison of continuous and intermittent training impact on glucose-4 transporter protein level and insulin sensitivity in diabetic rats

“…The increased insulin sensitivity after exercise occurs simultaneously with the accumulation of muscle glycogen stores (11). It is believed that increased muscle glycogen stores after exercise is due to increased GLUT4 (12,13) and increased GLUT4 protein displacement from inside the cell to plasma surface (13). The findings of some studies show that exercise (36,37) may impact on AMPK activity and AMPK impact on protein GLUT4 (37).…”

“…The increased insulin sensitivity occurs after exercise simultaneously with accumulation of muscle glycogen stores (11). It is believed that the increased muscle glycogen stores after the exercise is due to increased GLUT4 (12,13) and increased GLUT4 protein translocation from inside the cell to plasma surface [13]. In this context, Park et al (2011) reported the increased GLUT4 in skeletal muscle of healthy and diabetic mice after 6 weeks running on a treadmill at a speed of 15 meters per minute (14).…”

The vignette for V12N6 issue

“…Glycogen-depleting exercise is found to increase expression of the proteins that govern glucose uptake in skeletal muscle, including GLUT4 and mitochondrial enzyme activity [22]. Chou et al [23] therefore studied the effect of exerise and insulin administration on muscle glycogen storage and regulation of GLUT4 protein expression. Exercise induces GLUT4 protein expression and glucose tolerance in rats, but this stimulatory effect is abolished by glycogen overload induced by postexercise insulin administration.…”