If peripheral changes in GLP‐1 are detected at the OB following a meal, fasting or as a consequence of a metabolic disease state (hypothesis 2–3), or if odour signalling pathways release GLP‐1 in the OB locally (hypothesis 1), GLP‐1 sensitive potassium currents are capable of enhancing the AP firing frequency of the major output neurons or lowering their threshold for excitability. Here, GCG is linked to metabolic disease.