Glucagon-like peptide 1 (GLP-1) and GLP-1 analogs have received much recent attention due to the success of GLP-1 mimetics in treating type II diabetes mellitus (T2DM), but these compounds may also have the potential to treat obesity. The satiety effect of GLP-1 may involve both within-meal enteroenteric reflexes, and across-meal central signaling mechanisms, that mediate changes in appetite and promote satiety. Here, we review data supporting the role of both peripheral and central GLP-1 signaling in the control of gastrointestinal motility and food intake. Understanding the mechanisms underlying the appetite-suppressive effects of GLP-1 may help in developing targeted treatments for obesity.