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Insights into Brown Adipose Tissue Functions and Browning Phenomenon

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Brown adipose tissue (BAT), a thermogenic organ receiving considerable attention for its intrinsic capacity to increase energy expenditure and contribute to whole body energy balance, is now attracting new interest. Functional BAT is present in adult humans, where its quantity and activity correlate ...

Brown adipose tissue (BAT), a thermogenic organ receiving considerable attention for its intrinsic capacity to increase energy expenditure and contribute to whole body energy balance, is now attracting new interest. Functional BAT is present in adult humans, where its quantity and activity correlate positively with resting metabolic rate while being negatively correlated with BMI. The natural function of BAT is non-shivering thermogenesis. This occurs due to the peculiar presence of mitochondrial UCP1 that uncouples the oxidation of fuel substrates from the production of ATP, thus generating heat.

Aside from thermogenic contributions to energy expenditure, the beneficial effects of brown activation involve: i) the UCP1 independently enhanced mitochondrial oxidative machinery ii) the new, inadequately explored function as antioxidative defence and iii) the active channelling of systemic metabolite substrates, improving dyslipidemic, hyperglycemic and acidosis conditions. In addition, the emerging concept of a specific brown fat secretoma provides a physiologically significant link between adipose and systemic metabolism. These recent discoveries highlight the relevance of research concerning the physiological and the pharmacological tools that promote BAT activity.

Brown adipocytes are found in discrete areas in murine and human BAT, whereas clusters of UCP-1 expressing adipocytes are dispersed in white adipose tissue (WAT). Chronic cold exposure or β3-AR agonists treatment stimulate the formation of these new brown-like cells (brite/beige cells) because WAT and BAT undergo adaptive and dynamic changes in response to appropriate stimuli. In this context, the WAT remodelling (browning) has become an additional, attractive therapeutic target to increase energy expenditure. This is due to the mounting evidence suggesting that beige/brite cells are metabolically active, contributing to both thermogenesis and/or metabolic homeostasis.

Physiological stimuli, as well as hormonal, pharmacological and dietary determinants that could be linked to BAT activation and browning in WAT, have become a trending topic with important repercussions in the biomedical field. Cold has always been considered the main stimulus for BAT activation and recruitment, and the sympathetic nervous system is classically recognized as the main mediator of cold-induced BAT activation. Recently, a number of studies have demonstrated that lifestyle interventions such as nutritional strategies (microbiota) and physical activity (high aerobic capacity), could be considered new physiological stimuli for BAT activation and the browning phenomenon.

Interestingly, novel humoral and nutritional "factors" capable of activating brown cells through non-sympathetic mechanisms have been recently identified and have opened up possibilities for a new non-sympathetic approach to BAT activation. However, whether the physiological effects of these factors are direct or included in a sympathetic-mediated component is not completely clear and deserves further research.

This Research Topic aims to provide an integral physiological overview of BAT activation and the browning phenomenon. We suggest to focus on activators and physiological conditions recently found to regulate the browning process and to explore unexpected putative roles for brown/brite cells.
All interested researchers are welcome to submit review articles as well as novel findings (original papers) that give further insights into brown adipose physiology and develop a therapeutic strategy for the treatment and prevention of obesity and associate metabolic complications.


Keywords: thermogenesis, uncoupling proteins, mitochondria, obesity, metabolic syndrome


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