The main physiological function of brown and beige adipocytes is to control the amount of energy dissipated in form of heat required to maintain core body temperature, e.g. during cold exposure, a process known as non-shivering thermogenesis. 

Whether via direct uncoupling of ATP synthesis by UCP1 as mainly occurring in brown adipocytes, or by futile cycling of creatine, fatty acids, or calcium, as believed to dominate in beige thermogenic adipocytes, the guiding hypothesis is that expending more energy in the form of heat could be used to promote negative energy balance and prevent or reverse obesity. 

Furthermore, the expended substrate spectrum that fuels thermogenesis could be utilized to clear e.g. systemic glucose and thereby treat hyperglycemia in type 2 diabetes. 

While most current research in thermogenesis aims to identify activators of these processes, uncontrolled thermogenesis may produce excessive heat, promote cachexia, and muscular waste processes. 

Thus, physiological, and potentially pharmacologic brakes for thermogenesis are highly relevant and important as well. 

One of our projects here investigates one of our favorite proteins, the serpin vaspin. We have previously found that vaspin expression is specifically increased in activated BAT and unraveled underlying regulatory mechanisms [1]. We discovered that expression is highly induced in activated brown adipose tissue (BAT) in response to cold or energy-dense diets. We are now investigating the role of vaspin in BAT thermogenesis using a new human vaspin transgenic mouse model [2] as well as comprehensive proteomic and phospho-proteomic analysis to investigate also potentially protease-independent functions in thermogenic adipocytes.