Abstract
While exercise training (ET) is an efficient strategy to manage obesity, it is recommended with a dietary plan to maximize the antiobesity functions owing to a compensational increase in energy intake. Capsiate is a notable bioactive compound for managing obesity owing to its capacity to increase energy expenditure. We aimed to examine whether the antiobesity effects of ET can be further enhanced by capsiate intake (CI) and determine its effects on resting energy expenditure and metabolic molecules. Mice were randomly divided into four groups (n = 8 per group) and fed high-fat diet. Mild-intensity treadmill ET was conducted five times/week; capsiate (10 mg/kg) was orally administered daily. After 8 weeks, resting metabolic rate and metabolic molecules were analyzed. ET with CI additively reduced the abdominal fat rate by 18% and solely upregulated beta-3-adrenoceptors in adipose tissue (p = 0.013) but did not affect the metabolic molecules in skeletal muscles. Surprisingly, CI without ET significantly increased the abdominal fat rate (p = 0.001) and reduced energy expenditure by 9%. Therefore, capsiate could be a candidate compound for maximizing the antiobesity effects of ET by upregulating beta-3-adrenoceptors in adipose tissue, but CI without ET may not be beneficial in managing obesity.
Highlights
Accepted: 12 January 2021Obesity causes an endocrine imbalance that can lead to various metabolic disorders such as cardiovascular disease and type 2 diabetes [1]
At the beginning of the experiment, there was no significant difference in body weight (BW) among the groups
The purpose of this study was to examine whether the antiobesity effects of Exercise training (ET) can be further enhanced by capsiate intake (CI) via change in resting energy metabolism and to determine its effects on metabolic molecules in diet-induced obese mice
Summary
Obesity causes an endocrine imbalance that can lead to various metabolic disorders such as cardiovascular disease and type 2 diabetes [1]. This is because excess adipose tissue abnormally generates a large amount of cytokines and bioactive mediators, namely leptin and interleukin-6 [2]. A recent study found that this discrepancy, known as “weight compensation,” results primarily from a concomitant increase in appetite and subsequent increased energy intake, especially in response to long-term exercise [9]. This phenomenon has been reported in rodents [10]. It indicates that a dietary strategy may be necessary to maximize the antiobesity function of exercise especially in the long-
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