Unlike beta-cell insulin, its alpha-cell neighbor, glucagon, did not soar to sudden prominence. With no pressing need for a hyperglycemic agent, it offered little therapeutic promise beyond limited use in relieving hypoglycemic reactions. Thus, unprodded by urgent practical necessity, glucagon research proceeded at a leisurely pace. The pace is now accelerating, as recent studies disclose the hormone's importance in metabolism and its previously unsuspected therapeutic possibilities.
Glucagon exerts varied, far-reaching effects in the liver and other organs. In the liver it accelerates conversion of glycogen to glucose, triglyceride breakdown to free fatty acids, glucose formation from protein, and utilization of amino acids. In the pancreas it stimulates insulin secretion. Both in the liver and pancreas its effects are mediated by the enzyme adenyl cyclase and the associated cyclic adenosine 3′, 5′-monophosphate (c-AMP) system. Synthesized from adenosine triphosphate by the catalytic action of adenyl cyclase, c-AMP acts as a transmitter of
GLUCAGON IN CONGESTIVE HEART FAILURE. JAMA. 1968;206(5):1078. doi:10.1001/jama.1968.03150050066017