Volume 27, Issue 4 (6-2020)                   RJMS 2020, 27(4): 88-95 | Back to browse issues page

Research code: مقاله مستخرج از رساله دکتری است
Ethics code: متعهد مي شويم تا قبل از چاپ مقاله كد اخلاق درج گردد

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Islamic Azad University, Tehran, Iran , abednazari@gmail.com
Abstract:   (2525 Views)
Background: The aim of this study was to determine the effect of 12 weeks resistance training on G6Pase And PEPCK Gene Expression in Liver Hepatocytes, Glucose Levels And Beta- cells function in Type 2 Diabetic Rats. Type 2 diabetes is the most common endemic disease due to non-glucose intolerance, which affects the balance between reserves and insulin requirements. Several factors play a role in the development of this disease.Obesity increases the risk of developing the disease by increasing insulin resistance and increasing blood glucose levels. Also, other factors such as hormonal, genetic, metabolic and enzymatic disorders can also be effective in the development of type 2 diabetes.  In this regard, most studies have sought to understand how hormonal or metabolic factors affect insulin function and synthesize or release it from beta cells. But less attention has been paid to glucose production processes by some body tissues (such as liver) that especially in diabetic patients, lead to hyperglycemia .In fact, an increase in glucose, which is mainly due to increased glucose release, is a major feature of type 2 diabetes. The liver is one of the key mechanisms for maintaining and stabilizing the systemic glucose hemostasis in the body that is able to produce glucose by some pathways such as breaking glycogen (glycogenolysis) and the synthesis of glucose from non-carbohydrate precursors such as pyruvate, glycerol, lactate and alanine (gluconeogenesis). The rate of gluconeogenesis is controlled and regulated by the activity of some enzymes such as phosphoanol pyruvate carboxy kinase (PEPCK), fructose 1 and 6 diphosphatase, and glucose 6-phosphatase (G6Pase). This indicates the key role of these enzymes in the regulation of glucose hemostasis and thus diabetes . Also, the genetic coding of these proteins is strongly controlled by the transcription of certain key hormones, particularly insulin, glucagon, adrenaline (epinephrine), and glucocorticoids. Given the negative impact of diabetes on individual and social life, researchers are always looking for ways to minimize, prevent and treat diabetes. In this regard, various methods such as medication and various sports exercises have been used and contradictory conclusions have been obtained.
Methods: In this experimental study, 16 rats of the Wistar breed with a mean weight of 20 20 220 g were randomly divided into two groups of resistance training (n = 8) and control group (n = 8). The rats were injected with nicotinamide 95 mg / kg body weight and after 15 minutes STZ injection 55 mg / kg intraperitoneally. The training program used in this study included resistance training. In the resistance training group, 8 male Wistar 10-week-old diabetic rats participated in the training sessions for 12 weeks in 5 sessions per week in 3 courses with 6 repetitions per period. The Rest intervals between the courses was 3 minutes and the Rest intervals between repetitions in each period was 45 seconds.
The training program was as follows:
- In the first week, repetitions were performed with 10% of body weight.
- In the second and third weeks, repetitions were performed with 20% of body weight.
- In the fourth and fifth weeks, repetitions were performed with 40% of body weight.
- In the sixth and seventh weeks, repetitions were performed with 60% of body weight.
-In the eighth and ninth weeks, repetitions were performed with 80% of body weight.
- From the tenth to the twelfth week, repetitions were performed with 100% body weight. The control group also consisted of 8 male 10 week old male Wistar rats who were diabetic intraperitoneally injected and were not involved in any training program Finally,48 hours after the last exercise session, G6Pase And PEPCK gene expression in liver cells, glucose levels and beta- cells function were measured in both groups. Independent T-test was used for inferential analysis of the data.
Results: Findings in relation to gene expression showed that resistance training resulted in a significant reduction of expression of the G6Pase enzyme, glucose levels and increase Beta- cells function in the liver cells of the resistance group compared to the control group. These results are presented in Table 1.
Table 1. Relative expression of G6Pase, PEPCK expression, glucose levels and Beta- cells function in resistance and control groups
sig T test Mean difference df Number Exprimental Group Control Group statistical
0.01* 2.993 0.220 12 14 0/78(±0/19) 1 G6Pase expression
0.052 2.161 0.239 12 14 0.76±0.29 1 PEPCK expression
<0.0001* 9.989 81.00 12 14 213±18 1 glucose (mg/dl)
<0.0001* -9/405 -8/357 12 14 14/68±2/33 1 (HOMA-IR)
Conclusion: The results of the present study showed that resistance training to insulin resistance in type 2 diabetic rats did not have a significant effect. The mechanism of action of different types of exercise on glucose homeostasis is similar. Resistance training increases muscle mass and strength, thereby improving insulin sensitivity and glycemic control. Also, resistance training increases glucose uptake by active muscles and stimulates GLUT-4 and its transfer to the cell membrane, and rapid glucose uptake increases active skeletal muscle by protein carriers (34).
In the present study, resistance training seems to stimulate glucose metabolism and thus lead to changes in blood glucose levels. Because blood sugar is affected by hepatic glycogenolysis (due to the presence of the enzyme glucose phosphatase), it can be said that the intensity and duration of the resistance training program in the present study may have caused changes in the glycogenolysis process. However, the changes do not appear to be significant enough to lead to a significant change in insulin resistance, perhaps the duration of training should be changed to see a significant change in insulin resistance. Of course, these are speculations that need further research.
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Type of Study: Research | Subject: Exercise Physiology

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