Duration of Improved Muscle Glucose Uptake After Acute Exercise in Obese Zucker Rats

Betts, J. J.; Sherman, W. M.; Reed, Michael J.; Gao, Jiaping

doi:10.1002/j.1550-8528.1993.tb00624.x

Cited by 12 publications

(13 citation statements)

References 31 publications

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“…Examination of earlier studies reveals similar results (22,23,27,28), but these previous publications failed to identify mechanisms for this outcome. Results of the current study identified a plausible mechanism for this outcome by revealing that diet-related differences in insulin-stimulated GU postexercise were accompanied by greater pAS160 Ser588 and pAS160 Thr642 in muscles from LFD versus HFD rats independent of significant postexercise differences in proximal signaling.…”

Section: Discussionmentioning

confidence: 75%

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

et al. 2014

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Earlier research on rats with normal insulin sensitivity demonstrated that acute exercise increased insulin-stimulated glucose uptake (GU) concomitant with greater phosphorylation of Akt substrate of 160 kDa (pAS160). Because mechanisms for exercise effects on GU in insulin-resistant muscle are unknown, our primary objective was to assess insulin-stimulated GU, proximal insulin signaling (insulin receptor [IR] tyrosine phosphorylation, IR substrate 1–phosphatidylinositol-3-kinase, and Akt phosphorylation and activity), and pAS160 in muscles from acutely exercised (one session) and sedentary rats fed either chow (low-fat diet [LFD]; normal insulin sensitivity) or a high-fat diet (HFD; for 2 weeks, insulin-resistant). At 3 h postexercise (3hPEX), isolated epitrochlearis muscles were used for insulin-stimulated GU and insulin signaling measurements. Although exercise did not enhance proximal signaling in either group, insulin-stimulated GU at 3hPEX exceeded respective sedentary control subjects (Sedentary) in both diet groups. Furthermore, insulin-stimulated GU for LFD-3hPEX was greater than HFD-3hPEX values. For HFD-3hPEX muscles, pAS160 exceeded HFD-Sedentary, but in muscle from LFD-3hPEX rats, pAS160 was greater still than HFD-3hPEX values. These results implicated pAS160 as a potential determinant of the exercise-induced elevation in insulin-stimulated GU for each diet group and also revealed pAS160 as a possible mediator of greater postexercise GU of insulin-stimulated muscles from the insulin-sensitive versus insulin-resistant group.

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Section: Discussionmentioning

confidence: 75%

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

et al. 2014

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“…It is therefore unclear whether a single bout of exercise may influence insulin signaling cascade and myocardial insulin sensitivity. It was reported that a single bout of intermittent exercise ameliorated whole glucose tolerance for a short duration (b48 h), while insulin signaling cascade had no change in skeletal muscle [27]. Thus the time course of exercise-enhanced myocardial insulin sensitivity remains to be elucidated.…”

Section: Limitationsmentioning

confidence: 97%

Swim training sensitizes myocardial response to insulin: Role of Akt-dependent eNOS activation

Zhang

et al. 2007

Cardiovascular Research

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“…One exercise session can increase insulin-stimulated glucose disposal in insulin-resistant humans (9,23,24,88,103) and rats (2,14,40,84,95,114). Insulin-resistant humans and rats after acute exercise can reach glucose uptake values similar to healthy but unexercised controls (2,14,24,40,95).…”

Section: Improved Insulin-stimulated Glucose Uptake Postexercise In Imentioning

confidence: 99%

Mechanisms for greater insulin-stimulated glucose uptake in normal and insulin-resistant skeletal muscle after acute exercise

Cartee

2015

American Journal of Physiology-Endocrinology and Metabolism

104

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Enhanced skeletal muscle and whole body insulin sensitivity can persist for up to 24 -48 h after one exercise session. This review focuses on potential mechanisms for greater postexercise and insulinstimulated glucose uptake (ISGU) by muscle in individuals with normal or reduced insulin sensitivity. A model is proposed for the processes underlying this improvement; i.e., triggers initiate events that activate subsequent memory elements, which store information that is relayed to mediators, which translate memory into action by controlling an end effector that directly executes increased insulin-stimulated glucose transport. Several candidates are potential triggers or memory elements, but none have been conclusively verified. Regarding potential mediators in both normal and insulin-resistant individuals, elevated postexercise ISGU with a physiological insulin dose coincides with greater Akt substrate of 160 kDa (AS160) phosphorylation without improved proximal insulin signaling at steps from insulin receptor binding to Akt activity. Causality remains to be established between greater AS160 phosphorylation and improved ISGU. The end effector for normal individuals is increased GLUT4 translocation, but this remains untested for insulin-resistant individuals postexercise. Following exercise, insulin-resistant individuals can attain ISGU values similar to nonexercising healthy controls, but after a comparable exercise protocol performed by both groups, ISGU for the insulin-resistant group has been consistently reported to be below postexercise values for the healthy group. Further research is required to fully understand the mechanisms underlying the improved postexercise ISGU in individuals with normal or subnormal insulin sensitivity and to explain the disparity between these groups after similar exercise. insulin sensitivity; physical activity; glucose transporter 4; AMP-activated protein kinase; Akt substrate of 160 kDa Importance of Insulin-Stimulated Glucose Uptake by Skeletal MuscleUNDERSTANDING THE MECHANISMS regulating insulin-stimulated glucose uptake by skeletal muscle is important because 1) muscle accounts for most insulin-mediated glucose disposal (21) and 2) muscle insulin resistance is a key defect in the progression to type 2 diabetes mellitus (20,43,97). Even in nondiabetic individuals, insulin resistance increases the risk for atherogenesis, cardiovascular disease, hypertension, cognitive dysfunction, and some cancers (27,45,69).Insulin and exercise can independently increase glucose uptake secondary to redistribution of GLUT4 glucose transporters from the cell interior to cell surface membranes (CSM) (19,25,93). Elevated insulin-independent glucose uptake during exercise is mostly reversed by ϳ2-3 h postexercise, whereas enhanced muscle and whole body insulin sensitivity, detectable at ϳ1-4 h postexercise, can persist for up to 24 -48 h (1, 12, 13, 79, 88, 92, 124).Exercise capacity is related to muscle glycogen availability, and glycogen stores are diminished by vigorous exercise (59). Increase...

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Duration of Improved Muscle Glucose Uptake After Acute Exercise in Obese Zucker Rats

Cited by 12 publications

References 31 publications

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

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

Swim training sensitizes myocardial response to insulin: Role of Akt-dependent eNOS activation

Mechanisms for greater insulin-stimulated glucose uptake in normal and insulin-resistant skeletal muscle after acute exercise

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