Various peripheral neuropeptides regulate appetite and influence the development of obesity. Of these, ghrelin, or growth hormone- (GH-) releasing peptide, is the only known circulating orexigen, or appetite stimulant. Ghrelin is gut hormone. Ghrelin acts as a meal initiator as ghrelin levels rise prior to meals, and falls quickly after ingestion of nutrients. The ghrelin receptor, GH secretagogue receptor type 1a (GHS-R1a), is a G-protein coupled receptor. Exogenous ghrelin administration affects glucose homeostasis, gut motility, pancreatic exocrine secretion, cardiovascular function, immunity, and inflammation [89]. Administration of ghrelin to obese and lean human subjects leads to increased food intake, in part by stimulating the production of NPY and AgRP in the arcuate nucleus. Ghrelin may also alter energy balance by stimulating adipogenesis, inhibiting apoptosis, transitioning from fatty acid oxidation to glycolysis for energy expenditure, and inhibiting sympathetic nervous system activity. Future studies may examine ghrelin antagonists as a therapeutic option for obesity [90, 91]. The biological activities of ghrelin require octanoylation of the peptide on Ser3, a posttranslational modification that is catalyzed by the enzyme ghrelin O-acyltransferase (GOAT). GO-Coa-Tat, a peptide-based
