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Stimulatory regulators of glucagon release include hypoglycemia, amino acids and the gut hormone glucose-dependent insulinotropic peptide (GIP), whereas hyperglycemia and GLP-1 inhibit glucagon release. Glucagon secretion occurs as exocytosis of stored peptide vesicles initiated by secretory stimuli of the alpha cell. Glucagon release is regulated through endocrine and paracrine pathways by nutritional substances and by the autonomic nervous system ( 11). Glucagon is secreted in response to hypoglycemia, prolonged fasting, exercise and protein-rich meals ( 10). Since then it has become evident that glucagon not only acts by increasing hepatic glucose production but affects overall energy homeostasis in times of limited energy supply by stimulating lipid and protein catabolism, reducing appetite and food intake and increasing energy expenditure. It was discovered that patients with diabetes exhibit increased glucagon levels which led to the вЂњbihormonal hypothesisвЂќ stating that the combination of hypoinsulinemia and hyperglucagonemia constitutes a central pathophysiological determinant for diabetic hyperglycemia ( 7). The development of a radioimmunoassay for the detection of glucagon in 1959 spurred further investigations of glucagon physiology and its role in health and disease ( 6). This led to the development of medical use of glucagon for the treatment of severe insulin-induced hypoglycemia ( 4, 5). In the 1950s glucagon was purified and crystallized at Eli Lilly and Co., and shortly after, the amino acid sequence of the peptide was determined ( 3). The hyperglycemic effect of glucagon was described as early as 1922 by Kimball and Murlin who discovered a hyperglycemic factor in pancreatic extracts and called this factor вЂњthe glucose agonistвЂќ, hence the name glucagon ( 2). Accordingly, normal plasma glucose concentrations depend largely on the balanced secretion of insulin and glucagon from the pancreatic beta cells and alpha cells, respectively. In line with these opposed actions, high plasma glucose concentrations stimulating insulin secretion from pancreatic beta cells, inhibit glucagon secretion whereas low plasma glucose concentrations represent one of the most potent glucagon secretory stimuli. Thus, in contrast to the glucose-depositing nature of insulin action, glucagon acts as a glucose-mobilizing hormone. Glucagon secreted from pancreatic alpha cells in the islet of Langerhans plays an important role in maintaining glucose homeostasis by stimulating hepatic glucose production ( 1).

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For complete coverage of all related areas of Endocrinology, please visit our on-line FREE web-text, INTRODUCTION Finally, the role of glucagon in the pathophysiology of diabetes, obesity and hepatic steatosis is discussed and emerging glucagon-based therapies for these conditions are outlined. This chapter provides an overview of the structure, secretion, degradation and elimination of glucagon, and reviews the actions of glucagon including its role in glucose metabolism and its effects on lipolysis, ketogenesis, energy expenditure, appetite and food intake. Based on satiety-inducing and food intake-lowering effects of exogenous glucagon, a role for glucagon in the regulation of appetite has also been proposed.

However, glucagon is also involved in hepatic lipid and amino acid metabolism and may increase resting energy expenditure. Hypoglycemia is physiologically the most potent secretory stimulus and the best known action of glucagon is to stimulate glucose production in the liver and thereby to maintain adequate plasma glucose concentrations. Hicks Morley congratulates 35 of our lawyers for being recognized in the 2022 edition of The Best Lawyers in Canadaв„ў in the areas of Labour and Employment Law, Employee Benefits Law, Corporate and Commercial Litigation, and WorkersвЂ™ Compensation Law.Glucagon is a peptide hormone secreted from the alpha cells of the pancreatic islets of Langerhans. Hicks Morley Lawyers Recognized in the 2022 Edition of The Best Lawyers in Canadaв„ў

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