The body efficiently stores energy in the form of fat molecules. However, fats cannot directly enter or exit our cells, but first need to be degraded. This degradation process is tightly regulated to prevent the accumulation of fats either within organs or within the bloodstream - hallmarks of diseases such as obesity and cardiovascular disease. To exit our cells, stored fats need to be broken down to fuel organs in need of energy. We investigated the potential role of a promising new protein called HILPDA in the regulation of this breakdown process. To allow for uptake by underlying organs, fats are also efficiently broken down within the bloodstream. We characterized a protein called angiopoietin-like 4 (ANGPTL4) that acts a potent inhibitor of the fat breakdown in the bloodstream. In fact, we could show that different organs collaborate to
ensure that fats are appropriately distributed to organs in need of energy by adjusting the levels of ANGPTL4.