Abstract
Since the recent rediscovery of brown adipose tissue (BAT) in adult humans, this thermogenic tissue has been attracting increasing interest. The inverse relationship between BAT activity and body fatness suggests that BAT, because of its energy dissipating activity, is protective against body fat accumulation. Cold exposure activates and recruits BAT, resulting in increased energy expenditure and decreased body fatness. The stimulatory effects of cold exposure are mediated through transient receptor potential (TRP) channels and the sympathetic nervous system (SNS). Most TRP members also function as chemesthetic receptors for various food ingredients, and indeed, agonists of TRP vanilloid 1 such as capsaicin and its analog capsinoids mimic the effects of cold exposure to decrease body fatness through the activation and recruitment of BAT. The antiobesity effect of other food ingredients including tea catechins may be attributable, at least in part, to the activation of the TRP–SNS–BAT axis. BAT is also involved in the facultative thermogenesis induced by meal intake, referred to as diet-induced thermogenesis (DIT), which is a significant component of the total energy expenditure in our daily lives. Emerging evidence suggests a crucial role for the SNS in BAT-associated DIT, particularly during the early phase, but several gut-derived humoral factors may also participate in meal-induced BAT activation. One intriguing factor is bile acids, which activate BAT directly through Takeda G-protein receptor 5 (TGR5) in brown adipocytes. Given the apparent beneficial effects of some TRP agonists and bile acids on whole-body substrate and energy metabolism, the TRP/TGR5–BAT axis represents a promising target for combating obesity and related metabolic disorders in humans.
Highlights
Brown adipose tissue (BAT) has long been recognized as the major site of non-shivering thermogenesis (NST) during cold exposure [cold-induced thermogenesis (CIT)] and arousal from hibernation in small rodents [1]
When the participants were divided into high BAT and low BAT groups according to the result of FDG-positron emission tomography (PET)/computed tomography (CT) examination, there was no significant difference in body composition and resting EE between the two groups
One interesting development is a recent report by Leiria et al [98], who observed that administration of a β3 adrenergic receptor (β3AR) agonist induces a rapid increase in the plasma levels of 12- hydroxyeicosapentaenoic acid (12-HEPE) and 14-hydroxydocosahesanoic acids (14-HDHA), lipoxygenase products of EPA and docosahexaenoic acid (DHA), in parallel with the BAT activity assessed by FDG-PET/CT, in humans
Summary
Brown adipose tissue (BAT) has long been recognized as the major site of non-shivering thermogenesis (NST) during cold exposure [cold-induced thermogenesis (CIT)] and arousal from hibernation in small rodents [1]. Despite the abundance of evidence in rodents, the thermogenic effect of EPA and DHA and its relation to BAT in humans remain to be investigated In this context, one interesting development is a recent report by Leiria et al [98], who observed that administration of a β3AR agonist induces a rapid increase in the plasma levels of 12- hydroxyeicosapentaenoic acid (12-HEPE) and 14-hydroxydocosahesanoic acids (14-HDHA), lipoxygenase products of EPA and DHA, in parallel with the BAT activity assessed by FDG-PET/CT, in humans. One interesting development is a recent report by Leiria et al [98], who observed that administration of a β3AR agonist induces a rapid increase in the plasma levels of 12- hydroxyeicosapentaenoic acid (12-HEPE) and 14-hydroxydocosahesanoic acids (14-HDHA), lipoxygenase products of EPA and DHA, in parallel with the BAT activity assessed by FDG-PET/CT, in humans They demonstrated in mice that activated brown adipocytes released 12-HEPE to promote glucose uptake into skeletal muscle and adipose tissues. It seems possible that 12-HEPE is a BAT-derived factor that improves insulin sensitivity and glucose metabolism [21,22,23,24]
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