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RJMS 2020, 27 - : 46-56 |
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Research code: 118741/23
Ethics code: IR.SSU.REC.1398.511
Clinical trials code: IR.SSU.REC.1398.511
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Torabi H, Eizadi M, Jalalvand A, Zarinkalam E. The effect of long-term aerobic training on lipocalin2 expression in subcutaneous fatty tissue and insulin function in diabetic rats. RJMS 2020; 27 :46-56
URL: http://rjms.iums.ac.ir/article-1-6599-en.html
URL: http://rjms.iums.ac.ir/article-1-6599-en.html
Saveh Branch, Islamic Azad University, Saveh, Iran , izadimojtaba2006@yahoo.com
Abstract: (2363 Views)
Background & Aims: Although insufficient secretion of insulin from pancreatic beta cells or increased release of hepatic glucose are factors in the prevalence of type 2 diabetes, but insulin inefficiency in target tissues such as adipose tissue, liver and muscle is the most important factor in the disease in the form of increased insulin resistance or decreased Insulin sensitivity appears. Laboratory studies have also identified adipose tissue as one of the most important secretory areas of these mediators. Apart from adiponectin, leptin, resistin, TNF-α and IL-10, the effective role of lipocalin-2 as another adipose-secreted adipocytokine in insulin function and type 2 diabetes has been repeatedly suggested. As one of the most important members of the lipocalin family, lipocalin-2 peptide derived from adipose tissue as a biomarker of various diseases is also an effective factor in inflammatory responses related to metabolic disorders and a close relationship between its levels and adipose tissue has been observed. On the other hand, a significant relationship with fatty pancreas and a non-significant relationship with fatty liver has been observed. These findings suggest that increased synthesis and secretion of lipocalin-2 leads to the accumulation of fat in the pancreas, known as the fatty pancreas. Overall, these findings indicate a lack of general consensus on the role of lipocalin-2 on insulin resistance and sensitivity. However, modification of lipocalin-2 levels or its expression in target tissue in mice and humans leads to increased insulin sensitivity. Therefore, it seems that the invention of strategies to eliminate these shortcomings will reduce the severity of this disease. In this regard, it seems that therapeutic interventions that are able to improve lipocalin-2 function and lipocalin-2 expression in target tissues such as adipose tissue can provide a better understanding of the processes associated with their changes in reducing metabolic abnormalities or diseases Vascular are effective lead. It is well established that proper exercise or physical activity is associated with beneficial effects on metabolic or cardiovascular disease. However, there is evidence of conflicting responses to systemic levels or lipocalin-2 expression to exercise. Some studies have reported an increase in circulatory levels or expression of lipocalin-2 and others have decreased in response to exercise. Based on the evidence, the findings in this area depend on multiple factors such as the study population, pathological conditions, type of exercise (endurance, resistance), intensity of training (low, moderate, severe), duration of training (immediate, chronic, short-term, Long-term) and gender are different from each other. Therefore, in the present study, the effect of a course of aerobic exercise on lipokalin-2 expression in subcutaneous adipose tissue, as well as glucose levels and insulin resistance in type 2 diabetic rats were measured and the findings were discussed.
Methods: For this purpose, type 2 diabetes were induced in 14 male wistar rats 10 weeks (220 ± 20 g) by intraperitoneal injection of nicotine amide and STZ, then were randomly divided into exercise (aerobic training, 12 weeks, n = 7) or control (n = 7) groups. Aerobic training was performed 5 sessions weekly in the form of running on a rodent treadmill. Glucose level, insulin, insulin resistance and lipocalin 2 expression in subcutaneous adipose tissue were measured at 48 hours after lasting exercise in 2 groups. Independent t-test was used for comparing variables between groups.
Results: Aerobic training induced significant decrease in fasting glucose (p < 0.001), insulin resistance (p = 0.008) and lipocalin-2 expression in subcutaneous adipose tissue (p = 0.003) compared to the control group. On the other hand, serum insulin levels increased significantly in response to aerobic training compared to the control group (p = 0.009).
Conclusion: Decreased expression of lipocalin-2 in the subcutaneous adipose tissue of diabetic rats in response to the main aerobic exercise found in the present study. Also, aerobic exercise was associated with decreased glucose levels, increased serum insulin and decreased insulin resistance. Improving serum glucose and insulin can be attributed to a decrease in insulin resistance in response to aerobic exercise. On the other hand, based on the available evidence, the decrease in insulin resistance may be attributed to the decreased expression of lipocalin-2 in subcutaneous adipose tissue. Regarding glucose and insulin homeostasis in response to exercise, although contradictory findings are observable, often consistent results have been reported. Decreased lipocalin-2 in response to internal or external stimuli appears to be dependent on changes in other cytokines. In this regard, Samarra et al. (2009) first introduced IL-1B as a regulator of the function and expression of lipocalin-2 in adipose tissue. On the other hand, Mehrabani et al. (2014) attributed the decrease in lipocalin-2 in response to aerobic exercise to a decrease in IL-1B and introduced the improvement of insulin resistance as a result of the interaction between lipocalin-2 and IL-1B. Inflammatory cytokines TNF-α and INF-γ induce the expression and secretion of lipocalin-2 in adipose tissue. On the other hand, it has been suggested that lipocalin-2 has a kind of anti-inflammatory function by modulating the process of PPARy receptors to reduce the function of nuclear factor kappa (NF-kB). However, some researchers have attributed the decrease in fasting insulin and glucose resistance to the interaction of lipocalin 2 with hepatic insulin sensitivity rather than peripheral insulin sensitivity.
In conclusion, the secretion and expression of lipocalin-2 in adipose tissue is regulated by various stimuli such as insulin, fatty acids, insulin-dependent glucose uptake and cytokines, especially IL-1B, TNF-α and NF-κβ. It seems that the possible changes of each of these variables in response to exercise affect the secretion and expression of lipocalin 2 in adipose tissue. Among these, insulin-dependent glucose uptake has been introduced as one of the most important transcriptional stimulators of lipocalin 2. As fasting glucose and insulin levels decrease, increased fatty acids and norepinephrine play an important role in the secretion and induction of lipocalin-2 expression in adipose tissue. Therefore, it is hypothesized that reducing fasting levels of norepinephrine and fatty acids in response to exercise tends to reduce the secretion and expression of lipocalin-2 in laboratory rats.
Altogether, Based on these findings, it can be say that the improvement in blood glucose and insulin resistance in exercise group compared to the control is probably rooted in the reduction of lipocalin-2 expression in response to aerobic training. However, understanding the mechanisms responsible for improving glucose homeostasis in response to exercise training requires measuring other genetic and hormonal components.
Methods: For this purpose, type 2 diabetes were induced in 14 male wistar rats 10 weeks (220 ± 20 g) by intraperitoneal injection of nicotine amide and STZ, then were randomly divided into exercise (aerobic training, 12 weeks, n = 7) or control (n = 7) groups. Aerobic training was performed 5 sessions weekly in the form of running on a rodent treadmill. Glucose level, insulin, insulin resistance and lipocalin 2 expression in subcutaneous adipose tissue were measured at 48 hours after lasting exercise in 2 groups. Independent t-test was used for comparing variables between groups.
Results: Aerobic training induced significant decrease in fasting glucose (p < 0.001), insulin resistance (p = 0.008) and lipocalin-2 expression in subcutaneous adipose tissue (p = 0.003) compared to the control group. On the other hand, serum insulin levels increased significantly in response to aerobic training compared to the control group (p = 0.009).
Conclusion: Decreased expression of lipocalin-2 in the subcutaneous adipose tissue of diabetic rats in response to the main aerobic exercise found in the present study. Also, aerobic exercise was associated with decreased glucose levels, increased serum insulin and decreased insulin resistance. Improving serum glucose and insulin can be attributed to a decrease in insulin resistance in response to aerobic exercise. On the other hand, based on the available evidence, the decrease in insulin resistance may be attributed to the decreased expression of lipocalin-2 in subcutaneous adipose tissue. Regarding glucose and insulin homeostasis in response to exercise, although contradictory findings are observable, often consistent results have been reported. Decreased lipocalin-2 in response to internal or external stimuli appears to be dependent on changes in other cytokines. In this regard, Samarra et al. (2009) first introduced IL-1B as a regulator of the function and expression of lipocalin-2 in adipose tissue. On the other hand, Mehrabani et al. (2014) attributed the decrease in lipocalin-2 in response to aerobic exercise to a decrease in IL-1B and introduced the improvement of insulin resistance as a result of the interaction between lipocalin-2 and IL-1B. Inflammatory cytokines TNF-α and INF-γ induce the expression and secretion of lipocalin-2 in adipose tissue. On the other hand, it has been suggested that lipocalin-2 has a kind of anti-inflammatory function by modulating the process of PPARy receptors to reduce the function of nuclear factor kappa (NF-kB). However, some researchers have attributed the decrease in fasting insulin and glucose resistance to the interaction of lipocalin 2 with hepatic insulin sensitivity rather than peripheral insulin sensitivity.
In conclusion, the secretion and expression of lipocalin-2 in adipose tissue is regulated by various stimuli such as insulin, fatty acids, insulin-dependent glucose uptake and cytokines, especially IL-1B, TNF-α and NF-κβ. It seems that the possible changes of each of these variables in response to exercise affect the secretion and expression of lipocalin 2 in adipose tissue. Among these, insulin-dependent glucose uptake has been introduced as one of the most important transcriptional stimulators of lipocalin 2. As fasting glucose and insulin levels decrease, increased fatty acids and norepinephrine play an important role in the secretion and induction of lipocalin-2 expression in adipose tissue. Therefore, it is hypothesized that reducing fasting levels of norepinephrine and fatty acids in response to exercise tends to reduce the secretion and expression of lipocalin-2 in laboratory rats.
Altogether, Based on these findings, it can be say that the improvement in blood glucose and insulin resistance in exercise group compared to the control is probably rooted in the reduction of lipocalin-2 expression in response to aerobic training. However, understanding the mechanisms responsible for improving glucose homeostasis in response to exercise training requires measuring other genetic and hormonal components.
Type of Study: Research |
Subject:
Exercise Physiology
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