A previous study indicated that acyl ghrelin could enhance macrophage polarization to M1 directly in vitro, and deletion of its receptor GHSR in obese mice reduced macrophage infiltration, promoted macrophage polarization to M2 in adipose tissue, and suppressed adipose tissue inflammation (79); thus, these data suggest that Ghrelin/GHSR axis acts as an endocrine signal to induce a pro-inflammatory M1 phenotype in adipose tissue and that the deletion of GHSR promotes anti-inflammatory effects in obesity. Here, GHSR is linked to obesity disorder.