Endocrine Abstracts

The obesity epidemic has underlined the need for new treatments to aid weight loss and prevent the associated sequelae of obesity such as type 2 diabetes, hypertension, dyslipidaemia and cardiovascular disease. The relatively recent discovery of brown adipose tissue (BAT) in adult humans has revived interest in activating this tissue to increase energy expenditure as a novel treatment for obesity and associated metabolic disease. BAT is a thermogenic organ that generates heat to maintain body temperature in a cold environment. While BAT mass and activity are reduced in obesity, BAT is a plastic organ and activity can be increased in response to certain stimuli such as repeated cold exposure. In addition, the presence of BAT in obese subjects is associated with improved metabolic health and reduced incidence of cardiovascular disease. Therefore, it is important to determine how to safely increase BAT mass and thermogenesis to determine its therapeutic potential. However, our understanding of the pathways regulating human BAT remains limited, in part due to its location and the difficulty in quantifying activity in vivo. While most pharmacological agents known to activate BAT or increase browning have been identified in rodents, the majority have failed to translate to humans and there are key differences in the regulation of BAT activation between the species. The recent development of novel techniques to quantify human BAT activity in vivo has advanced our understanding of BAT thermogenesis and identified novel genes and pathways regulating thermogenesis, some with the potential for therapeutic manipulation. In this talk I will highlight these recent developments and discuss the potential of increasing energy expenditure as a treatment for obesity-associated metabolic disease.