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Endocrine Abstracts (2014) 34 S12.3 | DOI: 10.1530/endoabs.34.S12.3

University of Dundee, Dundee, UK.


The fundamental importance of insulin to glucose homeostasis is well recognized and most evident in type 1 diabetes where β-cell destruction and loss of endogenous insulin secretion lead to marked hyperglycaemia and ketosis. The pancreatic α-cell product, glucagon, has garnered less scientific attention. However, the demonstration that glucagon receptor null mice did not develop diabetes following near-complete chemical destruction of the pancreatic β-cell renewed interest in glucagon and its contribution to glucose homeostasis in health and disease. Therapies targeting glucagon secretion or action are currently undergoing clinical trials in both type-1 and -2 diabetes.

Glucagon stimulates hepatic glucose production through actions on gluconeogenesis and glycogenolysis. The liver is exquisitely sensitive to glucagon and hence any disruption glucagon secretion or actin has profound effects on glucose homeostasis. The regulation of glucagon secretion is complex and reflects the interplay between direct signalling molecules, intra- and extra-pancreatic signals and an extensive neural input. The relative importance of each of these modulatory signals is controversial. In this presentation, we will briefly discuss glucagon physiology before reviewing those intra-and extra-pancreatic systems that regulate glucagon secretion. We aim to address the question: ‘Does glucagon need the brain for its effects on blood glucose?’

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