The postprandial state is characterized by a storage of nutrients in the liver, muscle and adipose tissue for later utilization. In the case of a protein rich meal, amino acids (AA) stimulate glucagon secretion by the α-cell. The aim of the present study was to determine the impact of the rise in glucagon on AA metabolism, particularly in the liver. We used a conscious catheterized dog model to recreate a postprandial condition using a pancreatic clamp. Portal infusions of glucose, AA and insulin were used to achieve postprandial levels while portal glucagon infusion either maintained the basal level or increased it by 3 fold. The high glucagon infusion reduced the increase in arterial AA concentrations compared to the basal glucagon level (-23%, P<0.05). In the presence of high glucagon, liver AA metabolism shifted towards a more catabolic state with less protein synthesis (-36%) and increased net urea production (+52%). Net hepatic glucose uptake was reduced (-35%), in association with lower glycogen synthesis (-54%), and also in part because of a higher utilization of AA in gluconeogenesis. The phosphorylation of AMPK was increased by the high glucagon infusion (+40%) and this could be responsible for increasing the expression of genes related to pathways producing energy and lowering those involved in energy consumption. In conclusion, the rise in glucagon associated with a protein rich meal promotes a catabolic utilization of AA in the liver thereby opposing the storage of AA in proteins.