Majallah-i Dānishkadah-i ̒ulūm-i Pizishkī-i Niyshābūr (Aug 2018)

Investigation effect of 12-week High-Intensity Interval Training FOXO1 Gene Expression of Subcutaneous Adipose Tissue and Insulin Resistance in Type 2 Diabetic Rats

  • afzal almasi,
  • Laleh Behboudi tabrizi,
  • Mojtaba Izadi

Journal volume & issue
Vol. 6, no. 2
pp. 12 – 20

Abstract

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Background and Objectives: Studies have pointed to the possible role of FOXO1 in the pathogenesis of type 2 diabetes, due to the claim that it affects glycemic control and lipid metabolism. The aim of this study was to investigate the effect of 12 weeks of high-intensity interval (HIIT) on FOXO1 expression in subcutaneous adipose tissue, insulin resistance, insulin resistance, and blood glucose in type 2 diabetic rats. Materials and Methods: This is a fundamental and experimental research. The statistical population of this study is all male Wistar rats of Pasteur Institute of Iran. Among them, 14 male Wistar 10 week old rats weighing 220 ± 20 gr Randomized method was used to participate in the study. After a fasting night (12 hours), rats were diabetic by injection of nicotinamide and streptozotocin and divided into 2 groups of HIIT training and control. 12-week exercises were performed in 5 sessions of 30 minutes per week in the running of the treadmill with 1-minute repetitions and 2-minute active rest. The untrained diabetic group did not attend any exercise program. 48 hours after the last training session, the rats were anesthetized and slaughtered. A t-test was used for statistical analysis. Results: 12 weeks of periodic exercise decreased the relative expression of FOXO1 in comparison with the control group (P = 0.033). However, there was no significant difference in insulin resistance between the two groups (P = 0.921), but glucose and insulin decreased significantly with 12 weeks of periodic exercise (P = 0.001). Conclusion: 12 weeks of HIIT training leads to a decrease in blood glucose levels, despite the lack of insulin resistance in type 2 diabetic rats. This improvement can be attributed somewhat to signaling pathways dependent on changes in the expression of FOXO1 independent of insulin resistance.

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