Abstract
Obesity has become a global medical problem. The upregulation of senescence-related markers in adipose tissue may cause impairment of adipose tissue and disorders of systemic metabolism. Weight control through diet has been found to ameliorate senescence in the adipose tissue. Exercise is also important in maintaining a healthy lifestyle, however, very few researchers have examined the relationship between senescence-related markers in adipose tissue. Dietary restriction is also reported to have a legacy effect, wherein the effects are maintained for some periods after the termination of the intervention. However, very few researchers have examined the relationship between exercise and senescence-related markers in adipose tissue. Besides, there is no study on the long-term effects of exercise. Hence, we investigated whether the exercise could change the expression of senescence-related genes in the visceral adipose tissue of young mice and whether there was a legacy effect of exercise for 10 weeks after the termination of exercise. Four-week-old male ICR mice were assigned to one of the three groups: 20 weeks of sedentary condition, 20 weeks of voluntary wheel running exercise, or 10 weeks of exercise followed by 10 weeks of sedentary condition. The mice showed decreased expression in genes related to senescence and senescence-associated secretory phenotype, such as p53, p16, and IL-6, in the visceral adipose tissue in response to exercise. These effects were maintained for 10 weeks after the mice stopped exercising. Our study is the first report that exercise reduces the expression of senescence-related genes in the visceral adipose tissue of young mice, and that exercise causes the legacy effect.
Highlights
Imbalanced energy intake and eating disorders, induced by genetic and environmental factors, can cause overweight and even obesity [1]
Using the gene ontology (GO) analysis and the gene set enrichment analysis (GSEA), we found significant differences in a senescence-related gene set in the visceral adipose tissue between these two conditions (Table 1)
There was no significant difference in body weights between the Ex-Ex and Ex-Co groups
Summary
Imbalanced energy intake and eating disorders, induced by genetic and environmental factors, can cause overweight and even obesity [1]. Calle et al [2] reported that obesity increased the risk of death of patients with cardiovascular disease, cancer, or many other diseases. Schosserer et al [3] reviewed age-induced changes in white adipose tissue and concluded that aging caused a time-related decline in cells, organelles, tissues, and the organism that led to death. Tchkonia et al [4] reported that the number of senescent cells gradually increased in the adipose tissue of aging mammals. Muñoz-Espín et al [5] reviewed the accumulation of senescence cells in adipose tissue as one of the major drivers of aging and age-related disorders
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