Resistance training restores the gene expression of molecules related to fat oxidation and lipogenesis in the liver of ovariectomized rats.

Decreased levels of estrogen are associated with hepatic steatosis (HS), through changes in gene expression of molecules related to fat oxidation and lipogenesis. Both resistance training (RT) and endurance training (ET) prevent HS in ovariectomized (Ovx) rats. However, the molecular events associated with this process were only investigated for ET, but not for RT. Thus, the aim of this study was to investigate the effects of Ovx and RT on the gene expression of molecules related to fat oxidation and lipogenesis in the liver of rats. Sprague-Dawley adult female rats were grouped into four (n = 6 per group): sham-operated sedentary (Sham-Sed); Ovx sedentary (Ovx-Sed); sham-Rt and Ovx-Rt. A 10-week RT period, during which the animals climbed a 1.1-m vertical ladder with weights attached to their tails, was used. The sessions were performed three times a week, with 4-9 climbs and 8-12 dynamic movements per climb. Gene expression was analyzed by RT-PCR by the ∆∆Ct method. The estrogen deficiency associated with ovariectomy decreased the gene expression of molecules related to fat oxidation, carnitine palmitoyltransferase I (53%) and ß-hydroxyacyl-CoA dehydrogenase (27%), and increased molecules related to lipogenesis, sterol regulatory element-binding protein-1c (106%), acetyl-CoA carboxylase (ACC) (72%) and stearoyl CoA desaturase-1 (109%). With the exception of ACC, the ovariectomy-induced changes in the expression of these molecules were restored by RT. The present results indicate that RT has important effects on the prevention of HS in Ovx animals, through changes in gene expression of molecules related to hepatic lipid metabolism.

High-Intensity Interval Training Does Not Change Vaspin and Omentin and Does Not Reduce Visceral Adipose Tissue in Obese Rats.

This study aimed to determine the expression of omentin and vaspin, inflammatory markers, body composition, and lipid profile in diet-induced obese rats and high-intensity interval training (HIIT). Forty Wistar rats were divided into four groups: untrained normal diet, trained normal diet (T-ND), untrained high-fat diet (Unt-HFD), and trained high-fat diet (T-HFD). For the animals of the Unt-HFD and T-HFD groups, a high-fat diet was offered for 4 weeks. After that, all the animals in the T-ND and T-HFD groups were submitted to HITT, three times per week, for 10 weeks (2 weeks of adaptation and 8 weeks of HIIT). Muscle (gastrocnemius), liver, epididymal adipose tissue, retroperitoneal adipose tissue, visceral adipose tissue (VAT), and serum were collected to analyze TNF-α, IL-6, PCR, IL-8, IL-10, IL-4, vaspin, and omentin. A body composition analysis was performed before adaptation to HIIT protocol and after the last exercise session using dual-energy X-ray absorptiometry. Omentin and vaspin in the VAT were quantified using Western blotting. The results showed that, when fed a high-fat diet, the animals obtained significant gains in body fat and elevated serum concentrations of vaspin and blood triglycerides. The HIIT was able to minimize body fat gain but did not reduce visceral fat despite the increase in maximum exercise capacity. Moreover, there was a reduction in the serum levels of adiponectin, IL-6, and IL-10. Finally, we concluded that, although the training protocol was able to slow down the weight gain of the animals, there was no reduction in visceral fat or an improvement in the inflammatory profile, including no changes in omentin and vaspin.

Dietary Intervention, When Not Associated With Exercise, Upregulates Irisin/FNDC5 While Reducing Visceral Adiposity Markers in Obese Rats.

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.