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Glucose control of glucagon secretion: 'There's a brand-new gimmick every year'
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology.
2016 (English)In: Upsala Journal of Medical Sciences, ISSN 0300-9734, E-ISSN 2000-1967, Vol. 121, no 2, 120-132 p.Article, review/survey (Refereed) PublishedText
Abstract [en]

Glucagon from the pancreatic alpha-cells is a major blood glucose-regulating hormone whose most important role is to prevent hypoglycaemia that can be life-threatening due to the brain's strong dependence on glucose as energy source. Lack of blood glucose-lowering insulin after malfunction or autoimmune destruction of the pancreatic beta-cells is the recognized cause of diabetes, but recent evidence indicates that diabetic hyperglycaemia would not develop unless lack of insulin was accompanied by hypersecretion of glucagon. Glucagon release has therefore become an increasingly important target in diabetes management. Despite decades of research, an understanding of how glucagon secretion is regulated remains elusive, and fundamentally different mechanisms continue to be proposed. The autonomous nervous system is an important determinant of glucagon release, but it is clear that secretion is also directly regulated within the pancreatic islets. The present review focuses on pancreatic islet mechanisms involved in glucose regulation of glucagon release. It will be argued that alpha-cell-intrinsic processes are most important for regulation of glucagon release during recovery from hypoglycaemia and that paracrine inhibition by somatostatin from the delta-cells shapes pulsatile glucagon release in hyperglycaemia. The electrically coupled beta-cells ultimately determine islet hormone pulsatility by releasing synchronizing factors that affect the alpha- and delta-cells.

Place, publisher, year, edition, pages
2016. Vol. 121, no 2, 120-132 p.
Keyword [en]
Diabetes, glucagon secretion, glucose homeostasis, signal transduction
National Category
Family Medicine
URN: urn:nbn:se:uu:diva-299777DOI: 10.3109/03009734.2016.1154905ISI: 000376695600007PubMedID: 27044660OAI: diva2:950111
Swedish Research Council, 55X-06240Swedish Diabetes Association, DIA2014-071 DIA2015-027
Available from: 2016-07-27 Created: 2016-07-27 Last updated: 2016-07-27Bibliographically approved

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