Glycogen depletion and increased insulin sensitivity and responsiveness in muscle after exercise

Zorzano, A.; Balon, Thomas W.; Goodman, M. N.; Ruderman, Neil B.

doi:10.1152/ajpendo.1986.251.6.e664

Cited by 25 publications

(23 citation statements)

References 12 publications

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“…GLUT4 expression, but not GLUT1, was also increased in muscles with LG. Previous investigations have also reported fasting-induced increases in GLUT4 expression (5) and insulin-stimulated glucose uptake in skeletal muscles (18,44). GLUT4 is expected to transport the majority of glucose into skeletal muscles, and we find it likely that the elevated glucose uptake observed in muscles with LG, at least in part, is a consequence of increased GLUT4 expression.…”

supporting

confidence: 75%

Muscle glycogen inharmoniously regulates glycogen synthase activity, glucose uptake, and proximal insulin signaling

Jensen¹,

Jebens²,

Brennesvik³

et al. 2006

American Journal of Physiology-Endocrinology and Metabolism

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. Muscle glycogen inharmoniously regulates glycogen synthase activity, glucose uptake, and proximal insulin signaling. Am J Physiol Endocrinol Metab 290: E154 -E162, 2006. First published August 23, 2005 doi:10.1152/ajpendo.00330.2005.-Insulinstimulated glucose uptake and incorporation of glucose into skeletal muscle glycogen contribute to physiological regulation of blood glucose concentration. In the present study, glucose handling and insulin signaling in isolated rat muscles with low glycogen (LG, 24-h fasting) and high glycogen (HG, refed for 24 h) content were compared with muscles with normal glycogen (NG, rats kept on their normal diet). In LG, basal and insulin-stimulated glycogen synthesis and glycogen synthase activation were higher and glycogen synthase phosphorylation (Ser 645 , Ser 649 , Ser 653 , Ser 657 ) lower than in NG. GLUT4 expression, insulin-stimulated glucose uptake, and PKB phosphorylation were higher in LG than in NG, whereas insulin receptor tyrosyl phosphorylation, insulin receptor substrate-1-associated phosphatidylinositol 3-kinase activity, and GSK-3 phosphorylation were unchanged. Muscles with HG showed lower insulin-stimulated glycogen synthesis and glycogen synthase activation than NG despite similar dephosphorylation. Insulin signaling, glucose uptake, and GLUT4 expression were similar in HG and NG. This discordant regulation of glucose uptake and glycogen synthesis in HG resulted in higher insulin-stimulated glucose 6-phosphate concentration, higher glycolytic flux, and intracellular accumulation of nonphosphorylated 2-deoxyglucose. In conclusion, elevated glycogen synthase activation, glucose uptake, and GLUT4 expression enhance glycogen resynthesis in muscles with low glycogen. High glycogen concentration per se does not impair proximal insulin signaling or glucose uptake. "Insulin resistance" is observed at the level of glycogen synthase, and the reduced glycogen synthesis leads to increased levels of glucose 6-phosphate, glycolytic flux, and accumulation of nonphosphorylated 2-deoxyglucose. glucose transporter 4; protein kinase B; glycogen synthase kinase-3; phosphorylation; glucose metabolism; glycolytic flux; rat SKELETAL MUSCLE IS PARTICULARLY IMPORTANT in maintaining blood glucose homeostasis, as 70 -90% of insulin-stimulated glucose uptake occurs in skeletal muscle, where it is incorporated into and stored as glycogen (37). The glycogen concentration in skeletal muscles is limited, and a feedback mechanism exists. It has been 40 years since the classic study of Danforth (8), which showed that increased glycogen concentration reduced glycogen synthase activation in both the presence and absence of insulin. More recently, studies have shown that glycogen concentration also influences glucose uptake in skeletal muscles (2,9,17,18).Among the most important functions of insulin are stimulation of glucose uptake and activation of glycogen synthesis (35). Insulin stimulates glucose uptake in insulin responsive tissues by promoting translocation of the facilitative glucose t...

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supporting

confidence: 75%

Muscle glycogen inharmoniously regulates glycogen synthase activity, glucose uptake, and proximal insulin signaling

Jensen¹,

Jebens²,

Brennesvik³

et al. 2006

American Journal of Physiology-Endocrinology and Metabolism

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“…It might have been expected that exercise taken after breakfast would have affected glucose clearance also during the subsequent lunch. However, exerciseinduced enhancement of glucose clearance in the post exercise period is closely related to the depletion of muscle glycogen during exercise [28,29,31], and it wanes as glycogen stores are replenished by food intake [31]. The intensity and duration of exercise applied in the present study would even in the fasting state have been expected to result in only modest muscle glycogen breakdown.…”

Section: Discussionmentioning

confidence: 65%

“…1) (p < 0.05). The mechanism for this may include enhancement of both non-insulin and insulin-mediated glucose transport and disposal [28,29].…”

Section: Discussionmentioning

confidence: 99%

The effect of moderate exercise on postprandial glucose homeostasis in NIDDM patients

Larsen¹,

Dela²,

et al. 1997

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It is generally accepted that the metabolic regulation of non-insulin-dependent diabetic (NIDDM) patients is influenced by their diet and physical activity. In the postabsorptive state exercise of moderate intensity has been shown to decrease plasma glucose concentrations and is followed by an increase in insulin sensitivity [1][2][3][4][5]. Essentially these facts provide the rationale for using exercise as a tool in the treatment of NIDDM. However, during daily life physical exercise is mostly taken in the postprandial rather than in the postabsorptive state. In patients with insulin-dependent diabetes this fact has led to studies of the effect of exercise on postprandial glycaemia [4]. It was found that in patients treated with fixed Diabetologia (1997) Summary The influence of exercise on glycaemia in the post-prandial state was studied for the first time in non-insulin-dependent diabetic (NIDDM) patients. Meal-induced glucose responses were followed for 8 h in 9 diet-treated patients with NIDDM. Subjects consumed a standardized breakfast and 4 h later a standardized lunch. They were studied in the resting state (control day (CD)) and on another day 45 min of bicycle exercise (53 ± 2 % V O 2 max (mean ± SEM)) was performed 45 min after breakfast (exercise day (ED)). On day 3 (diet day (DD)), the breakfast meal was reduced corresponding to the extra energy expenditure during the exercise period on ED. Responses were calculated as areas under the plasma concentration curve (AUC) during 4 h after either breakfast (B-AUC) or lunch (L-AUC). B-AUC for glucose was identical on ED (215 ± 63 mmol/l ⋅ 240 min) and DD (219 ± 60 mmol/l ⋅ 240 min) and on these days lower (p < 0.05) than on CD (453 ± 78 mmol/l ⋅ 240 min). L-AUC for glucose on CD, ED and DD did not differ significantly.B-AUCs for both insulin and C-peptide were also significantly lower on ED and DD as compared to CD (Insulin: 31337 ± 8682, 26092 ± 6457 and 47649 ± 15046 mmol/l ⋅ 240 min, respectively. C-peptide: 99 ± 19, 104 ± 26 and 195 ± 31 pmol/ml ⋅ 240 min, respectively). Rate of appearance (Ra) for glucose was unaffected by exercise whereas rate of disappearance (Rd) increased significantly. No differences in Ra or Rd were observed after lunch. In conclusion, postprandial exercise of moderate intensity decreases glycaemia and plasma insulin levels after breakfast in NIDDM patients, but this effect does not persist during and after the following lunch meal. Reduction of breakfast caloric intake has the same effect on postprandial glycaemia and insulin secretion as an equivalent exercise-induced increase in caloric expenditure. [Diabetologia (1997) 40: 447-453] Keywords Insulin sensitivity, physical activity, insulin, C-peptide, non-esterified fatty acids; glycerol, glucose turnover.Received: 4 October 1996 and in revised form: 18 December 1996Corresponding author: J. J. S. Larsen, M. D., Department of Medical Physiology, The Panum Institute, Blegdamsvej 3, DK-2200 Copenhagen N, Denmark Abbreviations: CD, Control day; ED, exercise day; DD, diet day...

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“…Insulin sensitivity is defined as the concentration of insulin required to cause 50% of its maximal effect on glucose uptake, whereas insulin responsiveness is defined as the increase in glucose uptake induced by the maximally effective insulin concentration. Several previous studies reported that an acute bout of exercise enhanced insulin sensitivity in the skeletal muscles of fasted rats within 4 hours after the cessation of exercise, but that it failed to increase insulin responsiveness [7,10,11]. On the other hand, insulin responsiveness was reduced in the muscles of fed rats as compared with fasted rats.…”

Section: Introductionmentioning

confidence: 93%

Effect of acute high-intensity intermittent swimming on post-exercise insulin responsiveness in epitrochlearis muscle of fed rats

et al. 2009

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Glycogen depletion and increased insulin sensitivity and responsiveness in muscle after exercise

Cited by 25 publications

References 12 publications

Muscle glycogen inharmoniously regulates glycogen synthase activity, glucose uptake, and proximal insulin signaling

Muscle glycogen inharmoniously regulates glycogen synthase activity, glucose uptake, and proximal insulin signaling

The effect of moderate exercise on postprandial glucose homeostasis in NIDDM patients

Effect of acute high-intensity intermittent swimming on post-exercise insulin responsiveness in epitrochlearis muscle of fed rats

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