Postprandial GLP-1 release is attenuated in obese individuals (Näslund et al., 1998) and higher levels of GLP-1 appear to be required to produce anorectic effects and terminate a meal (Näslund et al., 1999), suggesting obesity-induced GLP-1 insensitivity, or “resistance” with regards to feeding outcomes. Here, GCG is linked to obesity due to melanocortin 4 receptor deficiency.