Advances in clinical research on glucagon.

Diabetol Int

Department of Endocrinology and Metabolism, Nagasaki University Hospital, 1-7-1 Sakamoto, Nagasaki, 852-8501 Japan.

Published: July 2024

AI Article Synopsis

  • The text marks the 100th anniversary of the discovery of glucagon, a key hormone that raises glucose levels and plays a role in amino-acid metabolism in the liver.
  • It discusses how glucagon's secretion by α-cells might adapt in response to metabolic disorders for maintaining metabolic balance.
  • The paper highlights advancements in clinical research on glucagon, particularly since 2014, when new methods enabled accurate measurements of its levels in the human body.

Article Abstract

We are now celebrating the 100th anniversary of the discovery of an important pancreatic hormone, glucagon. Glucagon is historically described as a diabetogenic hormone elevating glucose levels via increases in insulin resistance and hepatic gluconeogenesis. The more recently identified actions of glucagon include not only its pathophysiologic effects on glucose metabolism but also its significant roles in amino-acid metabolism in the liver. The possibility that abnormalities in α-cells' secretion of glucagon in metabolic disorders are a compensatory adaptation for the maintenance of metabolic homeostasis is another current issue. However, the clinical research concerning glucagon has been considerably behind the advances in basic research due to the lack of suitable methodology for obtaining precise measurements of plasma glucagon levels in humans. The precise physiology of glucagon secretory dynamics in individuals with metabolic dysfunction (including diabetes) has been clarified since the development in 2014 of a quantitative measurement technique for glucagon. In this review, we summarize the advances in the clinical research concerning glucagon, including those of our studies and the relevant literature.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11291794PMC
http://dx.doi.org/10.1007/s13340-024-00705-wDOI Listing

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