|Asprosin was first reported in 2016 as a fasting-induced protein hormone that modulates hepatic glucose. It is released as the C-terminal cleavage product of profibrillin (P35555). It is secreted by white adipose, circulates at nanomolar levels, and is recruited to the liver, where it activates the G protein-cAMP-PKA pathway, resulting in rapid glucose release into the circulation. The molecular mechanism is unknown but it is suggested asprosin uses a cell-surface receptor system distinct from those used by glucagon and catecholamines . A study published in 2017 suggests that in addition to performing a glucogenic function, asprosin is a centrally acting orexigenic hormone that is a potential therapeutic target in the treatment of both obesity and diabetes . The authors have also filed a patent claiming the potential use of asprosin (or an antobody or inhibitor of asprosin) for the maintenance of optimal body weight and blood glucose .