Razi Journal of Medical Sciences

 
Background: Abdominal obesity has been shown to be associated with increased impairment of glucose and insulin homeostasis and changes in blood lipid and lipoprotein levels such as low-density lipoprotein (LDL) and high-density lipoprotein (HDL). On the other hand, increasing fat activates some factors involved in the lipogenic pathway, such as the enzyme acetyl coenzyme A carboxylase, which is involved in fat metabolism. In this regard, one of the cases that has long been considered by researchers to reduce the negative effects of obesity is exercise and physical activity. Regular exercise can be an adjunct in the treatment of diseases caused by inactivity and obesity such as insulin resistance, diabetes and cardiovascular disease. But what exercise, for how long and with what intensity has the greatest impact is a question that has always attracted the attention of researchers.
On the other hand, one of the methods that has been considered in recent years along with exercise and physical activity is the use of pharmaceutical and dietary supplements such as octapamine, which has a structure similar to noradrenaline. And may modulate normal and abnormal neurophysiological processes and have stimulus-like properties that affect athletic performance.
Therefore, considering the effect of obesity and visceral fat in individual and social life, the role of lipogenic pathway and its effective factors on obesity, the possible effect of octapamine on physical activity on the one hand and on lipolysis on the other and finding a way to reduce the negative effects of obesity In the present study, the researcher sought to investigate whether aerobic activity associated with octapamine use affected the effect of aerobic exercise and octapamine supplementation on ACC and ACYL gene expression and HDL / LDL ratio in visceral adipose tissue of DFO-receiving rats. No?
Methods: In the present experimental study, 30 mice weighing 320 20 20 after one week of exposure to the new environment were randomly divided into 5 groups: healthy (6 mice), sick (DFO) (6 mice), Patient + octapamine (6 mice), patient + exercise (6 mice), patient + exercise + octapamine (6 mice) were divided and the exercise protocol was performed in such a way that the mice were first treated for one Week and 5 sessions per week at a speed of 10 meters, for 5 minutes and a zero degree slope of the introductory course, then the training groups, 5 sessions per week for 30 minutes of their training program. Out of a total of 30 minutes of training, 5 minutes were considered for warming up and 5 minutes for cooling. The research protocol was that on the first day of training, the speed started from 16 meters per second and increased every week until the last day and after 4 weeks, it reached 26 meters per second. It should be noted that the slope of the treadmill was zero degrees and moderate intensity training was performed in the range of 50 to 60% VO2max.
Also, 81 μmol / kg octapamine (Sigma Aldrich Company) dissolved in 9% normal saline was dissolved in the homogenase apparatus and per 100 g body weight of rats was injected intraperitoneally for 4 weeks and 5 times a week. At 4 weeks, an octopamine insulin line was injected subcutaneously.
On the other hand, in order to prepare oil heated several times, 8 liters of sunflower oil was heated for 190 consecutive hours at a temperature of 190 to 200 ° C for 4 consecutive days, and every 30 minutes food: chicken nuggets, potatoes, chicken and Protein products (sausages) were dipped in oil. Finally, the oil of the fourth day for use as an oral poisoning intervention (gavage) for 4 weeks every day at a rate of 10% of rat weight orally and by gavage to subjects in all groups except the group It was eaten healthy.
48 hours after the last training session and 8 hours of fasting, all rats were anesthetized by intraperitoneal injection of ketamine (75 mg / kg body weight) and xylazine (5 mg / kg body weight) And visceral adipose tissue was removed by HLE method. Finally, descriptive statistics, Shapiro-Wilk tests, two-way analysis of variance and Bonferroni post hoc test were used to analyze the data.
Results: The results of the present study showed that exercise, octapamine intake and the interaction between exercise and octapamine had a significant effect on HDL / LDL and ACYL in rat visceral adipose tissue. It was also found that HDL / LDL at the end of the period was significantly higher in the group fed with deep-training oil than the control group but the amount of ACYL was lower than the control group (Figures 1 and 3).
Another finding showed that exercise had a significant effect on ACC in visceral adipose tissue of rats. But octapamine intake and exercise-octapamine interaction had no significant effect on ACC gene expression in visceral adipose tissue. Also, the level of ACC at the end of the period was significantly higher in the group fed with deep heated oil-exercise than the control group (Figure 2).
Conclusion: Exercise seems to increase lipolysis and decrease fatty acids in the blood and muscles. This causes a layer of excess fat (cholesterol and phospholipids) that is transferred to HDL and causes it to increase. Increased HDL due to increased production by the liver may be due to altered LPL enzyme activity and decreased hepatic lipase following physical activity. Octapamine also activates b3-ARs and stimulates lipolysis in white fat cells, causing oxygen consumption in brown adipose tissue. It has also been reported that synephrine in octapamine is able to activate lipolysis in human adipocytes.
Regarding ACC, it can be said that the evidence shows that ACC is a key enzyme in regulating the biosynthesis of fatty acids in animal tissues. ACC acts as a lipid speed limiting enzyme. Acetyl coenzyme A carboxylase with carboxylation of acetyl coenzyme A causes the production of malonyl coenzyme A and it seems that the activity of acetyl coenzyme A carboxylase is affected by nutritional conditions. More and longer administration time will lead to a significant reduction in ACC. Regarding exercise-induced ACC regulation mechanisms, AMP-activated protein kinase (AMPK) has been shown to phosphorylate ACC in Ser79 and reduce its activity.