Thus, it appears that the paradoxal reduction of the orexigenic AcG in obesity might be a feedback mechanism to increased dietary caloric intake but not necessarily a pathophysiologic correlate for a reduced orexigenic capability of ghrelin, as this could be determined rather by the AcG/UnG ratio than by the absolute AcG levels. The gene discussed is GHRL; the disease is obesity due to melanocortin 4 receptor deficiency.