L'étrange histoire du glucagon

It was observed that dogs administrated insulin-enriched pancreas extract had a biphasic blood glucose response. In 1922, John Raymond Murlin attributed the initial rise in blood glucose followed by the expected glucose lowering to a substance which was later shown to be glucagon. The availability of pure crystalline glucagon led to the establishment of its hyperglycemic properties via the stimulation of glycogenolysis and gluconeogenesis in liver, and lipolysis in fat. As shown by Sutherland and de Duve, these actions were mediated by the stimulation of cyclic AMP, the “second messenger”. In 1957, Bromer determined that glucagon was a peptide of 29 amino-acids. The development by Unger of a radioimmunoassay permitted numerous studies showing that glucagon is a critical hormone for glucose homeostasis during fasting and exercise. Glucagon was shown as an antihypoglycemic agent. Later on, it was established that individuals with diabetes have inappropriately elevated levels of glucagon which may worsening the physiological derangements of diabetes.