Diabetes is a mild chronic inflammatory disease characterized by increased levels of circulating inflammatory agents secreted by adipose tissue called adipokines (2). Inflammation of adipose tissue is an important feature of adipose tissue disorder in obese people that is involved in the pathogenesis of related diseases such as insulin resistance and type 2 diabetes (3). Proinflammatory molecules produced in adipose tissue lead to the activation of intracellular signaling pathways (4). Among inflammatory molecules, MCP-1 is one of the major adipokines that initiates the penetration of adipose tissue macrophages and systemic insulin resistance (6). MCP-1 enhances the migration and transport of inflammatory cells by activating integrin and chemotaxis. It has been observed that MCP-1 expression in adipose tissue and plasma levels of MCP-1 is positively regulated by the degree of obesity. In addition, increased expression of this chemokine in adipose tissue precedes the expression of other macrophage markers during the spread of obesity (6). MCP-1 messaging also plays a direct role in the spread of obesity (7).In general, research suggests that lifestyle interventions such as exercise and diet can be helpful in managing diabetes. In addition, it has been shown that different methods of exercise have different effects on glycemic control in diabetic patients (7).
However, there is still no general consensus on the best way to exercise to affect diabetics. Therefore, according to the above and the proven role of various sports exercises in reducing the amount of adipose tissue in human and animal samples (10) and on the other hand due to increasing insulin sensitivity and reducing insulin resistance as a result of exercise and their different effects. On MCP-1 (11) and the close relationship between insulin resistance and increase in concentration and expression of MCP-1 (12) Has not been. Therefore, identifying the molecular mechanisms that govern adaptations stimulated by the three methods of exercise in adipose tissue and the regulatory mechanisms that improve adipose tissue metabolism can be therapeutically useful for maintaining health or treating disease.
2.MethodsThe present study was experimental in terms of implementation and fundamental in terms of purpose. For this study, 45 8-week-old male rats were randomly divided into 4 groups: resistance training (10 heads), endurance training (10 pieces), combination training (10 heads) and control training (10 heads). Rats were injected with nicotinamide (95 mg / kg body weight of saline) and after 15 minutes STZ injection (55 mg / kg body weight, prepared in sodium citrate buffer with pH). = 4/7) became diabetic subcutaneously. Rats in control groups received the same amount of buffer. 5 days after injection using a glucometer, rats with serum glucose between 300 and 360 mg / dL were considered diabetic.
In the present study, it was found that there is a significant difference between the effect of six weeks of endurance, resistance and combination exercise on protein monoacetate monocyte protein-1 (MCP-1) in the visceral adipose tissue of male diabetic mice. On the other hand, it was found that there was a significant difference between the effect of all three training programs with the control group, which showed that every three days of training on the protein content of NLRP-3 (Inflamasoma) in the visceral adipose tissue of diabetic male mice. It was also found that there is no significant difference between the three training methods, however, the results showed that endurance training is more effective than Turkish and resistance training. Consistent with the findings of the present study, Kazemi (2016) showed that MCP-1 levels of visceral and subcutaneous fat and plasma insulin decreased following intense intermittent exercise (7). Moderate-intensity exercise has been reported to reduce peripheral inflammatory markers, including MCP-1 (16). Based on our knowledge, the present study has for the first time investigated the effect of three methods of endurance training, resistance training and combination on MCP-1 in diabetic rats. Also, one of the possible mechanisms of MCP-1 reduction in the present study may be related to the role of IL-8 and osulin resistance in diabetics. However, more research is needed to determine the exact mechanism by which physical activity affects MCP-1. On the other hand, systemic administration of MCP-1 in mice has been shown to induce insulin resistance. Research has also shown that MCP-1 is mainly produced by macrophages, endothelial cells and adipocytes and acts as an adsorbent of macrophages in adipose tissue in obesity-dependent insulin resistance and atherogenesis (9). Therefore, there seems to be a direct relationship between MCP-1 levels and insulin resistance, and considering the decrease in insulin resistance in the present study, the reduction of MCP-1 also seems reasonable.Ethical Considerations