Postexercise Improvement in Insulin-Stimulated Glucose Uptake Occurs Concomitant With Greater AS160 Phosphorylation in Muscle From Normal and Insulin-Resistant Rats

Castorena, Carlos M.; Arias, Edward B.; Sharma, Naveen; Cartee, Gregory D.

doi:10.2337/db13-1686

Cited by 80 publications

(166 citation statements)

References 50 publications

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“…Previous in vitro studies showed that 2 or 4 wk of HFD feeding impairs insulin-stimulated glucose uptake in skeletal muscle after endurance exercise in rats (18,19). We found that blood glucose levels at 120 min after exercise were significantly higher in the HFD group than in the Con group.…”

Section: Discussionsupporting

confidence: 43%

“…Post-exercise glucose uptake in skeletal muscle is activated in an insulin-independent manner (contraction per se) and an insulin-dependent manner. A previous study showed that 2 wk of HFD intake did not affect the stimulation of glucose uptake in skeletal muscle induced by exercise with no insulin condition (19). Therefore, it is possible that pre-exercise HFD consumption for 3 d did not affect insulin-independent but only insulin-dependent glucose uptake during postexercise recovery.…”

Section: Discussionmentioning

confidence: 88%

“…Previous studies, which showed that HFD feeding for 2 or 4 wk impairs insulin-stimulated glucose uptake in skeletal muscle, did not measure glycogen levels in the fed state during post-exercise recovery (18,19). As it should be usual that subjects consume carbohydrates after exercise to stimulate glycogen recovery, we provided the mice with a glucose solution orally during their recovery from endurance exercise.…”

Section: Discussionmentioning

confidence: 99%

“…Insulin resistance in skeletal muscle induced by an HFD is associated with lower phosphorylated levels of the insulin signaling cascade (19,32,33); conflicting results were observed in post-exercise skeletal muscle of mice which were provided HFD for 2 or 4 wk (18,34). We determined total amounts and phosphorylation states of proteins which were involved in glucose uptake and glycogen synthesis after post-exercise glucose administration.…”

Section: Levels and Phosphorylated States Of Proteins Involved In Insmentioning

confidence: 99%

“…However, whether the short-term adaptation to high-fat diet (HFD) influences glycogen repletion in skeletal muscle after exercise has not been elucidated. Previous studies showed that HFD feeding for a longer period (2 or 4 wk) impairs insulinstimulated glucose uptake in skeletal muscle, which is a major rate-limiting step for glycogen synthesis, after endurance exercise in rats (18,19). In addition, HFD intake for 2-5 d attenuates blood glucose disposal during a glucose tolerance test (20,21) and insulin sensitivity during a hyperinsulinemic-euglycemic glucose clamp (22,23) in both humans and rodents, while some studies reported that HFD intake for 3 d does not affect glucose uptake in skeletal muscle at rest (24,25).…”

mentioning

confidence: 99%

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Pre-Exercise High-Fat Diet for 3 Days Affects Post-Exercise Skeletal Muscle Glycogen Repletion

Takahashi

Matsunaga

Tamura

et al. 2017

J Nutr Sci Vitaminol

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Summary Previous studies have shown that the short-term intake of a high-fat diet (HFD) impairs glucose metabolism. In this study, we investigated the influences of pre-exercise HFD intake for 3 d on post-exercise glycogen repletion in skeletal muscle in ICR mice. Mice received either an HFD (57% kcal from fat, 23% kcal from carbohydrate; HFD group) or standard laboratory chow (13% kcal from fat, 60% kcal from carbohydrate; Con group) for 3 d before exercise. Mice performed treadmill running at 25 m/min for 60 min and were orally administered a glucose (2 mg/g body weight) solution immediately after and at 60 min after exercise. A negative main effect of pre-exercise HFD intake was observed for skeletal muscle glycogen concentration from the pre-exercise phase to 120 min of post-exercise recovery (p,0.01). Blood glucose concentration in the HFD group was significantly higher than in the Con group at 120 min after exercise (p,0.01). No significant difference was observed in plasma insulin concentration. There were no significant between-group differences in the phosphorylation state of Akt Thr308, AMPK Thr172, AS160 Thr642, or glycogen synthase Ser641 or in glucose transporter 4 protein levels during post-exercise recovery. Our results suggest that the intake of a pre-exercise HFD for 3 d affects post-exercise glycogen repletion in skeletal muscle without impairing the insulin signaling cascade. Key Words skeletal muscle, post-exercise recovery, high-fat diet, glucoseThe pre-exercise glycogen store in skeletal muscle is considered a major determinant of exercise performance during moderate-to high-intensity exercise (1-4). When exercise intensity exceeds around 60-65% VO2max, the skeletal muscle glycogen store is the predominant source of energy (5, 6). Moreover, recent studies suggest that glycogen per se is important for skeletal muscle force production by the modulating excitationcontraction coupling process (7). When individuals are involved in multiple training sessions and competitions over successive days or within a day, enhancing glycogen repletion in skeletal muscle after exercise is essential for improving performance during subsequent exercise.Some athletes alter their dietary composition of carbohydrate and fat for several days to enhance their exercise performance. For example, adaptation to a ketogenic diet, which severely restricts carbohydrate intake (,20 g/d or 5% of total daily energy intake) and contains high fat levels and an adequate amount of protein, has been shown to be useful for weight control without detrimental effects on skeletal muscle mass, power output, or strength after not only long-term (.2 wk) but also short-term (7 d) administration (8-10). Adaptation to a ketogenic diet increases fat utilization and reduces carbohydrate reliance during exercise without impairing endurance capacity at 62-64% VO 2max under a state of insufficient carbohydrate availability (overnight fasting) (11). However, as a ketogenic diet sometimes causes side effects, including increased perceived exertio...

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Section: Discussionsupporting

confidence: 43%

Section: Discussionmentioning

confidence: 88%

Section: Discussionmentioning

confidence: 99%

Section: Levels and Phosphorylated States Of Proteins Involved In Insmentioning

confidence: 99%

mentioning

confidence: 99%

See 3 more Smart Citations

Pre-Exercise High-Fat Diet for 3 Days Affects Post-Exercise Skeletal Muscle Glycogen Repletion

Takahashi

Matsunaga

Tamura

et al. 2017

J Nutr Sci Vitaminol

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Role of AMP-Activated Protein Kinase for Regulating Post-exercise Insulin Sensitivity

Kjøbsted

Wojtaszewski

Treebak

2016

Experientia Supplementum

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Skeletal muscle insulin resistance precedes development of type 2 diabetes (T2D). As skeletal muscle is a major sink for glucose disposal, understanding the molecular mechanisms involved in maintaining insulin sensitivity of this tissue could potentially benefit millions of people that are diagnosed with insulin resistance. Regular physical activity in both healthy and insulin-resistant individuals is recognized as the single most effective intervention to increase whole-body insulin sensitivity and thereby positively affect glucose homeostasis. A single bout of exercise has long been known to increase glucose disposal in skeletal muscle in response to physiological insulin concentrations. While this effect is identified to be restricted to the previously exercised muscle, the molecular basis for an apparent convergence between exercise- and insulin-induced signaling pathways is incompletely known. In recent years, we and others have identified the Rab GTPase-activating protein, TBC1 domain family member 4 (TBC1D4) as a target of key protein kinases in the insulin- and exercise-activated signaling pathways. Our working hypothesis is that the AMP-activated protein kinase (AMPK) is important for the ability of exercise to insulin sensitize skeletal muscle through TBC1D4. Here, we aim to provide an overview of the current available evidence linking AMPK to post-exercise insulin sensitivity.

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Mechanism of Skeletal Muscle Contraction: Role of Mechanical Muscle Contraction in Glucose Homeostasis

Furuichi

2016

Musculoskeletal Disease Associated With Diabetes Mellitus

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Postexercise Improvement in Insulin-Stimulated Glucose Uptake Occurs Concomitant With Greater AS160 Phosphorylation in Muscle From Normal and Insulin-Resistant Rats

Cited by 80 publications

References 50 publications

Pre-Exercise High-Fat Diet for 3 Days Affects Post-Exercise Skeletal Muscle Glycogen Repletion

Pre-Exercise High-Fat Diet for 3 Days Affects Post-Exercise Skeletal Muscle Glycogen Repletion

Role of AMP-Activated Protein Kinase for Regulating Post-exercise Insulin Sensitivity

Mechanism of Skeletal Muscle Contraction: Role of Mechanical Muscle Contraction in Glucose Homeostasis

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