A combination of exercise and capsinoid supplementation additively suppresses diet-induced obesity by increasing energy expenditure in mice

Abstract

Exercise effectively prevents the development of obesity and obesity-related diseases such as type 2 diabetes. Capsinoids (CSNs) are capsaicin analogs found in a nonpungent pepper that increase whole body energy expenditure. Although both exercise and CSNs have antiobesity functions, the effectiveness of exercise with CSN supplementation has not yet been investigated. Here, we examined whether the beneficial effects of exercise could be further enhanced by CSN supplementation in mice. Mice were randomly assigned to four groups: 1) high-fat diet (HFD, Control), 2) HFD containing 0.3% CSNs, 3) HFD with voluntary running wheel exercise (Exercise), and 4) HFD containing 0.3% CSNs with voluntary running wheel exercise (Exercise ϩ CSN). After 8 wk of ingestion, blood and tissues were collected and analyzed. Although CSNs significantly suppressed body weight gain under the HFD, CSN supplementation with exercise additively decreased body weight gain and fat accumulation and increased whole body energy expenditure compared with exercise alone. Exercise together with CSN supplementation robustly improved metabolic profiles, including the plasma cholesterol level. Furthermore, this combination significantly prevented diet-induced liver steatosis and decreased the size of adipocyte cells in white adipose tissue. Exercise and CSNs significantly increased cAMP levels and PKA activity in brown adipose tissue (BAT), indicating an increase of lipolysis. Moreover, they significantly activated both the oxidative phosphorylation gene program and fatty acid oxidation in skeletal muscle. These results indicate that CSNs efficiently promote the antiobesity effect of exercise, in part by increasing energy expenditure via the activation of fat oxidation in skeletal muscle and lipolysis in BAT.exercise; capsinoids; obesity; energy expenditure; fat oxidation OBESITY IS RAPIDLY BECOMING a major global health problem (4) and is a major risk factor for several common diseases, including type 2 diabetes, cardiovascular diseases, and cancer (32). Obesity develops when energy intake chronically exceeds total energy expenditure (51). Conventional antiobesity strategies have focused on repressing energy intake by suppressing appetite or inhibiting intestinal fat absorption; however, increasing energy expenditure by activating the metabolic function of skeletal muscle or brown fat could serve as an alternative and effective antiobesity intervention, thereby avoiding the potential adverse effects associated with conventional antiobesity therapies such as depression, oily bowel movements, and steatorrhea.Exercise is one of the most efficient ways to prevent obesity and type 2 diabetes through an increase in energy expenditure (25, 27, 52). However, people in the developed world are becoming less physically active as a result of lifestyle changes and the nature of their work. Moreover, constraints such as lack of time, limited access. and injuries frequently become barriers to exercise (48). For example, a recent epidemiological study estimated that ...

Evaluation of Cyclic Adenosine Monophosphate and Neurotransmitters in Experimental Obesity: Impact of Black Pepper and Coffee Aqueous Extracts

“…Contrarily, serum cAMP levels were decreased in obese groups when compared to control group. These results were in agreement with Ohyama et al [43], who reported that the serum level of cAMP in obese was significantly lower than the non-obese rats. This may be due to the increase of FFAs and increased serum levels of mediators such as TNF-α, IL-1, IL-6, and NF-κB and reduced peroxisome proliferator-activated receptor gamma expression, resulting in overall decrease of serum cAMP [6].…”

Capsinoids suppress diet-induced obesity through uncoupling protein 1-dependent mechanism in mice

“…In this study, we investigated the role of UCP1 in the anti-obesity effect of capsinoids by using WT and UCP1-KO mice. Consistent with previous reports (Ohyama et al, 2015), chronic treatment with capsinoids suppressed increases in body weight and body fat accumulation induced by HFD feeding of WT mice. Capsinoids showed no effect on the body weight gain or WAT weight increase of UCP1-KO mice fed HFD, indicating that the fat-reducing effect of capsinoids is mediated by UCP1.…”

“…For example, a single oral administration of capsinoids increases oxygen consumption in mice (Kawabata et al, 2009;Ohnuki et al, 2001) and humans (Inoue, Matsunaga, Satoh, & Takahashi, 2007;Josse et al, 2010). Chronic treatment with capsinoids reduces body fat in mice (Ohnuki et al, 2001) and humans (Faraut et al, 2009;Snitker et al, 2009) and prevents high-fat diet-induced obesity (Ohyama et al, 2015). In addition, several studies have suggested the involvement of BAT or UCP1 in the effect of capsinoids.…”

Curcumin treatment enhances the effect of exercise on mitochondrial biogenesis in skeletal muscle by increasing cAMP levels

“…It is well known that exercise increases the levels of cAMP [33] and curcumin has also been reported to have this effect as measured by inhibition of endothelial cell phosphodiesterase (PDE) [34]. Curcumin indeed increased cAMP levels ( …”