NR3C1 and lipodystrophy: Vpr, an HIV protein responsible for viral replication that plays a multifactorial role by inhibiting the peroxisome proliferator-activating receptor-γ (PPARγ) and stimulating the glucocorticoid receptor (GR) and the liver X receptor-a (LXR-α), leads to preadipocyte differentiation, dysregulation, and the overaccumulation of FFA, while it also decreases hepatic fatty acid oxidation and reduces hepatic VLDL-TG exportation, ultimately leading to lipodystrophy [32,33,34,35,36].