Glucagon is also known as glucagon or anti insuli or insuli B. It is accompanied by a hormone insuli secretion from pancreatic islet alpha cells of vertebrates. Confrontation and insuli plays a role, increase blood glucose. In 1953, was isolated by precipitation and obtain the crystallization. It is based on the N- terminal histidine as a starting point, C terminal threonine is a single chain peptide terminus of 29 amino acids (molecular weight is about 3500), does not have the S-S bonds in a molecule, at this point, completely different from insuli. The structure of the compound has been synthesized by chemical recent affirmation. The early effect of glucagon process is specific binding exists in the target cell receptors on the cell membrane, the adenylate cyclase activation, ring type AMP as the second messenger activating phosphorylase, promoting glycogenolysis.

In contrast to the action of insuli, glucagon is a promoting hormone catabolism. Glucagon has very strong promoting glycogenolysis and gluconeogenesis, make the blood glucose increased significantly, 1mol/L hormone can make 3 x 106mol/L glucose from glycogen decomposed rapidly out. Glucagon by cAMP-PK system, the activation of hepatic cells accelerated glycogen phosphorylase, decomposition. Gluconeogenesis is enhanced because hormone accelerate amino acids into liver cells, and activate the enzyme of gluconeogenesis.

Glucagon also activates lipase, promote fat decomposition, and can enhance the oxidation of fatty acid, so that increased ketogenesis. The target organ of glucagon produced the metabolic effects of the liver, liver resection or interruption of hepatic blood flow, these effects disappeared.

In addition, the secretion of glucagon may promote insuli and islet somatostatin. Pharmacological doses of glucagon can make the content of cAMp in myocardial cells increased, myocardial contraction enhancement.