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Effect of an Aerobic Exercise Course on PI3K and AKT1 Expression and Neural Muscle Insulin Resistance in Diabetic Rats
Author(s) -
Mahdi Nadi,
Abdolali Banaeifar,
Sajad Arshadi
Publication year - 2021
Publication title -
iranian journal of diabetes and obesity
Language(s) - English
Resource type - Journals
eISSN - 2345-2250
pISSN - 2008-6792
DOI - 10.18502/ijdo.v13i3.7190
Subject(s) - medicine , aerobic exercise , analysis of variance , insulin resistance , endocrinology , diabetes mellitus , streptozotocin , treadmill , insulin , significant difference , protein kinase b , apoptosis , chemistry , biochemistry
Objective: The purpose of the present study was to investigate eight weeks of aerobic workout on PI3K and AKT expression as well as insulin resistance (IR) of muscle in diabetic rats by nicotinamide - streptozotocin. Materials and Methods: This laboratory study was conducted on 14 male Wistar rats (8 to 10 weeks) with a weight range of 201 to 250 g and induction of type 2 diabetes (one week). These mice were classified into 2 groups: aerobic training and control group. No exercise was given to the control group during the study, while the aerobic exercise program was run for 5 weeks a week with a gradual increase of speed (10 to 25 m / min) and time (15 to 40 minutes) in running treadmill was performed for the aerobic training group. Assay of gene expression in both study groups was by rt-PCR. For statistical analysis, the SPSS 19 software was used. The variables were compared between the two groups using one-way ANOVA. Results: The findings showed that there was no significant difference between the two groups in terms of IR in diabetic rats (3.85 (± 0.39) vs. 5.26 (± 0.55); P-value= 0.345). The expression of AKT (2.37 (± 2.33) vs. 1.000 (± 0.001); P-value= 0.042) and PI3K (2.87 (± 2.54) vs. 1.000 (± 0.001); P-value= 0.028) in the neural muscle of the training group compared with control group had a significant increase. Conclusion: It seems that performing eight weeks of aerobic exercise could be a strong stimulus for PI3K and AKT gene expression.

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