Abstract
This study aimed to investigate the influence of childhood exercise and detraining on brown adipose tissue (BAT) whitening in obesity. Four-week-old male Long-Evans Tokushima Otsuka (LETO) rats (n = 9) and Otsuka Long-Evans Tokushima Fatty (OLETF) rats (n = 24) were used as non-obese and obese animals, respectively. OLETF rats were divided into non-exercise sedentary (n = 9) and exercise groups. OLETF rats in the exercise group were further divided into subgroups according to the exercise period—exercise from 10- to 12-weeks-old (n = 6); and exercise from 4- to 6-weeks-old, and detraining from 6- to 12-weeks-old (n = 9). At 12-weeks-old, immediately after exercise period, BAT whitening in OLETF rats was inhibited by exercise despite the fact that hypertrophy was not caused in the plantaris muscle. However, the effectiveness was attenuated during the detraining period. Histological BAT whitening and downregulation of uncoupling protein-1 (UCP-1) were found in non-exercise sedentary OLETF rats at 12-weeks-old. The downregulation was not inhibited, even though exercise histologically inhibited BAT whitening in OLETF rats. Childhood exercise decreased BAT whitening in obesity. Detraining attenuated the inhibition of BAT whitening. These results suggest that regular exercise is needed to improve BAT whitening and downregulation of UCP-1 in obesity.
Highlights
Adipose tissues are composed of two major types: white adipose tissue (WAT) and brown adipose tissue (BAT), which have different features
The purpose of this study was to investigate the influence of childhood exercise and detraining on BAT whitening in obesity
The results of the present study revealed that childhood exercise inhibits BAT whitening in obesity
Summary
Adipose tissues are composed of two major types: white adipose tissue (WAT) and brown adipose tissue (BAT), which have different features. White and brown adipocytes are histologically characterized as containing unilocular and multilocular lipid droplets, respectively [1]. Heat production in BAT depends on the activity of uncoupling protein-1 (UCP-1) [3,4]. UCP-1 is localized in the inner mitochondrial membrane and acts as an uncoupler of oxidative phosphorylation and adenosine triphosphate (ATP) synthesis, thereby dissipating energy as heat [5,6]. The transformation of the lipid depot from multilocular to unilocular has been reported in brown adipocytes in obesity; the change from BAT to WAT is known as whitening [7,8]. Previous studies have reported that BAT whitening is associated with downregulation of mitochondrial proteins [10,11]. Downregulation of mitochondrial proteins induced by BAT whitening decreases the expression of
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