Effects of High-Intensity Aerobic Training and Myo-Inositol Supplementation on the Expression of AMPKα, Prkaa1, Prkaa2, and Akt Genes Associated with AMPK and Akt Signaling Pathways in Adipose Tissue of Obese Rats
Abstract
Obesity is one of the most prevalent metabolic disorders worldwide and is associated with profound alterations in energy regulation, insulin resistance, and metabolic diseases. Among the molecular pathways involved in metabolic homeostasis, the AMPK and Akt signaling pathways play critical roles in regulating energy balance and cellular metabolism. Dysregulation of genes related to these pathways may contribute to obesity-associated metabolic impairments. Therefore, the present study aimed to investigate the effects of high-intensity aerobic training and myo-inositol supplementation on the expression of AMPKα, Prkaa1, Prkaa2, and Akt genes in the adipose tissue of obese rats. In this experimental study, fifty male Wistar rats were rendered obese through a high-fat diet and randomly assigned to five groups: healthy control, obese control, high-intensity aerobic training, myo-inositol supplementation, and combined high-intensity aerobic training plus myo-inositol supplementation. The training intervention was performed for eight weeks, five sessions per week, while myo-inositol was administered concurrently throughout the intervention period. Gene expression levels were assessed using Real-Time PCR, and data were analyzed using one-way and two-way analyses of variance. The results demonstrated that obesity significantly reduced the expression of AMPKα, Prkaa1, Prkaa2, and Akt genes. High-intensity aerobic training significantly increased the expression of AMPK pathway-related genes, whereas myo-inositol exerted a more pronounced effect on Akt gene expression. Furthermore, the combined intervention produced the greatest increase in the expression of all investigated genes. These findings suggest that the combination of high-intensity aerobic training and myo-inositol supplementation may serve as an effective non-pharmacological strategy for improving gene expression patterns associated with energy regulation and metabolic function under obese conditions.
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