Glucagon is believed to cause hyperglycemia by promoting glycogenolysis in the liver. This is based on the following evidence which has been reviewed in detail recently (1) and which is largely indirect: 1) the hyperglycemic response to glucagon is decreased or absent in fasting, untreated diabetes, severe liver disease (2) and after evisceration ( 3 ) when the amount of liver glycogen is presumably low or absent; 2 ) glucagon is more effective when injected into the portal vein than by any other route of administration and is ineffective after occlusion of the liver circulation(2) ; 3) glucagon causes a sharp increase in splanchnic glucose production. as measured by venous catheterization in man ( 4 ) : 4) destruction of the pancreatic alpha cells, presumably accompanied by the liberation of preformed glucagon, causes an immediate hyperglycemia with a decrease in liver glycogen( 5 ) ; 5) glucagon promotes liver glycogenolysis in vitru by activating the phosphorylase system ( 6 ) . Although these findings would lead one to expect a decrease of liver glycogen in intact animals treated with glucagon, this effect has not been clearly demonstrated. Burger and Kramer(2) first reported a decrease in liver glycogen in dogs treated with glucagon. However, these pioneering results were obtained with crude preparations of glucagon heavily contaminated with insulin. Furthermore liver glycogen was determined in samples obtained by means of repeated biopsies, a traumatizing technic which may cause glycogenolysis in itself. Similarly, using an impure preparation of glucagon, Heard et a L ( 7 ) obtained a decrease in liver glycogen in normal rats, while Milman et al.(8) obtained similar results in vit. E-deficient rats. In contrast with these findings, the
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