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 analog that antagonizes GOAT inhibits GOAT in vitro, in cultured cells, and in mice. Intraperitoneal administration of GO-Coa-Tat improves glucose tolerance and reduces weight gain in wild-type mice but not in ghrelin knockout mice [92], suggesting its beneficial metabolic effects are due to specific GOAT inhibition. In addition to ghrelin, many peripheral neuropeptides may also be associated with satiety. The list of satiety peripheral hormones is extensive. Important peripheral neuropeptides include cholecystokinin (CCK), peptide YY (PYY3-36), pancreatic polypeptide (PP), incretins, glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), amylin, and bombesin. These peripheral hormones regulate gastrointestinal functions such as motility, secretion, and absorption and provide feedback to the central nervous system on availability of nutrients and may play an important role in regulating energy intake.
