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Obesity is an epidemic disease and the expansion of adipose tissue, especially visceral fat, promotes the secretion of factors that lead to comorbidities such as diabetes and cardiovascular diseases. Thus, diet and exercise have been proposed as an intervention to reverse these complications. An adipocytokine, known as irisin, mediates the beneficial effects of exercise. It has been proposed as a therapeutic potential in controlling obesity. In view of the above, this paper attempts to determine the modulation of irisin, visceral adiposity and biochemical markers in response to dietary intervention and aerobic exercise. To do this, 52 diet-induced obese male Wistar rats were divided into the following four groups: high-fat diet and exercise (HFD-Ex); HFD-Sedentary (HFD-Sed); chow-diet and exercise (CD-Exercise); and CD-Sed. The exercise-trained group performed a treadmill protocol for 60 min/day, 3 days/week for 8 weeks. Body mass (BM), body fat (BF), fat mass (FM), and fat-free mass (FFM) were analyzed. Mesenteric (MES), epididymal (EPI), and retroperitoneal (RET) adipose tissue was collected and histological analysis was performed. Biochemical irisin, triglycerides, glucose, insulin and inflammatory markers were determined and, FNDC5 protein expression was analyzed. In this study, the diet was the most important factor in reducing visceral adiposity in the short and long term. Exercise was an important factor in preserving muscle mass and reducing visceral depots after a long term. Moreover, the combination of diet and exercise can enhance these effects. Diet and exercise exclusively were the factors capable of increasing the values of irisin/FNDC5, however it did not bring cumulative effects of both interventions. Prescriptions to enhance the obesity treatments should involve reducing visceral adiposity by reducing the fat content in the diet associated with aerobic exercise.

This study aims to analyze the effects of resisted, aerobic, and combined exercises on omentin levels in visceral adipose tissue and muscle of rats with experimental diabetes to verify whether these adipokines are related to the glucose pathway and inflammation process in this model. Male Wistar rats received a high-fat diet for 4 weeks and a low dose of streptozotocin (35 mg/kg) to induce experimental diabetes. After inducing diabetes, the animals were divided into 4 experimental groups (n = 10): diabetic control (C); resistance training (RT); aerobic training (AT); and combined training (CT). The groups were exercised for 12 weeks, 3 times/week, where: RT means the stair climbing protocol until exhaustion; AT is the 30 min/day reaching 20 m/min protocol, and CT is the combination of RT and AT. The AT group showed reduced retroperitoneal and mesenteric adipose tissue and abdominal fat deposits. Our study also showed a possible control of blood glucose, as well as decreased Interleukin 6 (IL-6) and C-reactive protein, increased circulating adiponectin and increased omentin in visceral adipose tissue. In addition, the AT group affected the glucose pathway by stimulating phosphorylation of Akt in muscle tissue. Omentin also showed a strong positive correlation with adiponectin and a moderate negative correlation with IL-6. Thus, our findings indicated that omentin in type 2 diabetes is changed by AT. Furthermore, increased omentin levels had a close association with the glucose pathway by stimulating phosphorylation of Akt in muscle tissue and with IL-6 in serum, suggesting that omentin is likely to have anti-inflammatory and protective action in experimental diabetes.

This study aims to analyze the effects of resisted, aerobic, and combined exercises on omentin levels in visceral adipose tissue and muscle of rats with experimental diabetes to verify whether these adipokines are related to the glucose pathway and inflammation process in this model. Male Wistar rats received a high-fat diet for 4 weeks and a low dose of streptozotocin (35 mg/kg) to induce experimental diabetes. After inducing diabetes, the animals were divided into 4 experimental groups (n = 10): diabetic control (C); resistance training (RT); aerobic training (AT); and combined training (CT). The groups were exercised for 12 weeks, 3 times/week, where: RT means the stair climbing protocol until exhaustion; AT is the 30 min/day reaching 20 m/min protocol, and CT is the combination of RT and AT. The AT group showed reduced retroperitoneal and mesenteric adipose tissue and abdominal fat deposits. Our study also showed a possible control of blood glucose, as well as decreased Interleukin 6 (IL-6) and C-reactive protein, increased circulating adiponectin and increased omentin in visceral adipose tissue. In addition, the AT group affected the glucose pathway by stimulating phosphorylation of Akt in muscle tissue. Omentin also showed a strong positive correlation with adiponectin and a moderate negative correlation with IL-6. Thus, our findings indicated that omentin in type 2 diabetes is changed by AT. Furthermore, increased omentin levels had a close association with the glucose pathway by stimulating phosphorylation of Akt in muscle tissue and with IL-6 in serum, suggesting that omentin is likely to have anti-inflammatory and protective action in experimental diabetes.