The Effect of Six Weeks Aerobic Training on Adipose Tissue Energy Homeostasis Index in Obese Diabetic Rats

Message:
Article Type:
Research/Original Article (دارای رتبه معتبر)
Abstract:
Background & Aims

There is a close relationship between obesity and type 2 diabetes, so that the risk of developing type 2 diabetes in obese people is higher than people with normal weight (2, 3). Both type 2 diabetes and obesity are associated with changes in the body's metabolism, which is a determining factor in the development of insulin resistance (4, 5). Studies show that adipose tissue is a central metabolic organ in regulating energy homeostasis throughout the body and plays an important role in the development of insulin resistance and type 2 diabetes (6). It also secretes various hormones, cytokines, and metabolites that control systemic energy balance by regulating appetite signals from the central nervous system and metabolic activity in peripheral tissues (8). One of the peptide hormones expressed by various body tissues, including adipose tissue in animal and human samples, is adropin, which is involved in energy homeostasis, metabolic adaptation, and modulation of insulin sensitivity and obesity (9).Increased adropin levels have been reported following aerobic exercise (17). also, Abbasian et al. (2016) observed increase in serum adropin levels in overweight and obese men after 8 weeks of intense intermittent exercise (18). However, in the study of Alizadeh et al. (2015) following a session of aerobic exercise, no significant change in glucose and adropin factors was observed in overweight women (19).The effects of exercise training on changes of factors involved in energy metabolism in obese diabetic subjects have been less studied, therefore, the present study intends to investigate the question of whether six weeks of aerobic training affect the on adipose tissue energy homeostasis index in obese diabetic rats?

Methods

This is an experimental study. This research was conducted on Wistar rats at Islamic Azad University, Marvdasht Branch. 32 obese male wistar rats (weight 320±20 gr) after induction of diabetes randomly were divided into 4 groups including obese control, shem (obese), obese diabetic, obese aerobic training - obese diabetic. Rats were exposed to a high-fat controlled diet in the form of pellets for 4 weeks to gain weight (20). In this study, the rats were type 2 diabetic using peritoneal injection nicotinamide-STZ (21). Aerobic training program was performed on treadmill 4 days a week with intensity of 70% VO2max for six weeks (22). Blood samples were used to measure fasting glucose by enzymatic colorimetric method with glucose oxidase technology by Pars Azmoun Tehran kit company. Insulin was measured by ELISA method using a laboratory kit (Demeditec insulin ELIZA DE2935, Germany). Insulin resistance index was measured after Calculated fasting glucose and fasting insulin concentrations using the homeostasis model (HOMA-IR) and according to the formula. Also, the amount of adropine in adipose tissue of rats was measured using a special kit (Phoenix Pharmaceuticals, Inc. USA) by ELISA method. Adropin level were measured using ELISA kit. Data were analyzed by One-way ANOVA and Tukey post hoc test at the P<0.05.

Results

Mean and standard deviation of variables in adipose tissue of different research groups are presented in Table 2. The results showed that the adropin level in adipose tissue in the obese diabetic group was significantly lower than the obese control group (P=0.001). Also, insulin resistance was significantly higher in the obese diabetic group than the obese control groups (P=0.004). Aerobic training was associated with significant increase of adropin in adipose tissue and decrease of insulin resistance in obese diabetic rats (P=0.001).

Conclusion

The findings of this study were consistent with the results of Previous research (17, 23, 24). Insulin resistance, fasting glucose and insulin have a negative correlation with adropin levels (29). In the present study, a negative relationship was observed between adropin levels of adipose tissue and insulin and insulin resistance index, which may be one of the effective factors in increasing adropin levels of adipose tissue after aerobic training in the obese-diabetic exercise group. The molecular mechanism by which fat causes insulin resistance is unclear. Inflammation due to lipid accumulation, inhibitory effect of fatty acid oxidation on glucose oxidation, and secretion of adipocytokines are all associated with the development of local and systemic insulin resistance (36). Improvements in insulin resistance following exercise may be due in part to the potential effect of adropine on vasodilation. This improvement can facilitate access to glucose and enhance glucose metabolism (9). There were some limitations in the present study, such as the lack of measurement of other indicators of associated with energy homeostasis and metabolic adaptation in adipose tissue. According to the results, it seems that Aerobic training may be able to help reduce the effects of obesity in diabetes by improving adropin levels in adipose tissue and insulin resistance.

Language:
Persian
Published:
Razi Journal of Medical Sciences, Volume:28 Issue: 12, 2022
Pages:
166 to 175
magiran.com/p2429596  
دانلود و مطالعه متن این مقاله با یکی از روشهای زیر امکان پذیر است:
اشتراک شخصی
با عضویت و پرداخت آنلاین حق اشتراک یک‌ساله به مبلغ 1,390,000ريال می‌توانید 70 عنوان مطلب دانلود کنید!
اشتراک سازمانی
به کتابخانه دانشگاه یا محل کار خود پیشنهاد کنید تا اشتراک سازمانی این پایگاه را برای دسترسی نامحدود همه کاربران به متن مطالب تهیه نمایند!
توجه!
  • حق عضویت دریافتی صرف حمایت از نشریات عضو و نگهداری، تکمیل و توسعه مگیران می‌شود.
  • پرداخت حق اشتراک و دانلود مقالات اجازه بازنشر آن در سایر رسانه‌های چاپی و دیجیتال را به کاربر نمی‌دهد.
In order to view content subscription is required

Personal subscription
Subscribe magiran.com for 70 € euros via PayPal and download 70 articles during a year.
Organization subscription
Please contact us to subscribe your university or library for unlimited access!