The time course of insulin, glucagon and GLP-1 secretion rates are demonstrated as functions the GLP-1 glucose sensitivity as controls, without shunting and normal low presinusoidal resistance (Figure 9A, 9C and 9E), and with portosystemic shunting and high presinusoidal resistance, as obtains in NASH (Figure 9B, 9D and 9F). This evidence concerns the gene GCG and metabolic dysfunction-associated steatohepatitis.