Abstract

ABSTRACTObjective:To investigate the effects of different intensities of acute exercise on insulin sensitivity and protein kinase B/Akt activity in skeletal muscle of obese mice.Methods:Swiss mice were randomly divided into four groups, and fed either a standard diet (control group) or high fat diet (obese sedentary group and obese exercise group 1 and 2) for 12 weeks. Two different exercise protocols were used: swimming for 1 hour with or without an overload of 5% body weight. The insulin tolerance test was performed to estimate whole-body sensitivity. Western blot technique was used to determine protein levels of protein kinase B/Akt and phosphorylation by protein Kinase B/Akt in mice skeletal muscle.Results:A single bout of exercise inhibited the high fat diet-induced insulin resistance. There was increase in phosphorylation by protein kinase B/Akt serine, improve in insulin signaling and reduce of fasting glucose in mice that swam for 1 hour without overload and mice that swan for 1 hour with overload of 5%. However, no significant differences were seen between exercised groups.Conclusion:Regardless of intensity, aerobic exercise was able to improve insulin sensitivity and phosphorylation by protein kinase B/Ak, and proved to be a good form of treatment and prevention of type 2 diabetes.

Highlights

  • Physical exercise increases insulin sensitivity independently of body mass reduction and changes in body composition.[1]. The major effect of exercise is the increase in intracellular proteins expression of insulin signaling pathway especially the glucose transport in skeletal muscle.[1,2,3]

  • That situation revealed the importance of this isoform for cellular survival.[6]. Akt2 knockout mice developed characteristics of type 2 diabetes mellitus that were crucial for maintenance of glycemia

  • This study investigated the effects of different intensities of acute exercise on insulin sensibility and Akt phosphorylation in skeletal muscle of obese mice

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Summary

Introduction

Physical exercise increases insulin sensitivity independently of body mass reduction and changes in body composition.[1]. Obese individuals and resistant to insulin have as common characteristics the problem in insulin signaling due to subclinical inflammatory process. This process shows a decrease in action of this hormone in target cells and is influenced by the presence of fasting hyperglycemia and hyperinsulinemia. Such metabolic changes are associated with a decrease in glucose uptake by skeletal muscle in response to insulin.[4]. That situation revealed the importance of this isoform for cellular survival.[6] Akt knockout mice developed characteristics of type 2 diabetes mellitus that were crucial for maintenance of glycemia. Animals with protein Akt absence had an impairment in brain development.[5,6,7,8]

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