Department of Exercise Physiology, Islamshahr Branch, Islamic Azad University, Islamshahr, Iran , yaser.kazemzadeh@yahoo.com
Abstract: (2869 Views)
Background: It has been observed that PGC-1α content decreases in type 2 diabetes. In addition, hypoxia has been introduced as a new therapeutic intervention in type 2 diabetes. Therefore, the aim of this study was to evaluate the effect of eight weeks of daily normobaric hypoxia (60 minutes) on PGC-1α content of soleus muscle, insulin resistance, and fasting glucose in type 2 diabetic rats.
Materials and methods: In this study, 24 male Wistar rats were divided into three groups: control, diabetic, and diabetic hypoxia. In diabetic groups, induction of diabetes was performed by HFD-STZ method. The plan consisted of eight weeks, five sessions per week and 60 minutes of exposure to normobaric hypoxia with 14.4% oxygen in the diabetic hypoxia group in each session. At the end, tissue and blood samples were extracted for analysis. Statistical analysis was performed by one-way analysis of variance.
Results: The results of analysis of variance showed a significant difference in all three variables (p=0.0001). The results of post hoc test indicated a significant difference in PGC-1α between control and diabetic groups (p=0.0001), between control and diabetic hypoxia (p=0.0001), and between diabetic and diabetic hypoxia (p=0.009). Also, the post hoc test among three groups showed a significant difference (p=0.0001) in variables of fasting glucose and resistance to insulin.
Conclusion: Due to the effect of normobaric hypoxia on the increase of PGC-1α, the decrease of fasting glucose, and resistance to insulin, normobaric hypoxia can be used as a new treatment strategy in type 2 diabetes.
FallahpourNooshabadi S, Kazemzadeh Y, Gorzi A. The effect of eight weeks of daily normobaric hypoxia (60 minutes) on PGC1α content of soleus muscle, insulin resistance, and fasting glucose in type 2 diabetic rats. EBNESINA 2020; 22 (4) :89-94 URL: http://ebnesina.ajaums.ac.ir/article-1-909-en.html