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Glucose regulation of glucagon secretion
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology.
2014 (English)In: Diabetes Research and Clinical Practice, ISSN 0168-8227, E-ISSN 1872-8227, Vol. 103, no 1, 1-10 p.Article, review/survey (Refereed) Published
Abstract [en]

Glucagon secreted by pancreatic alpha-cells is the major hyperglycemic hormone correcting acute hypoglycaemia (glucose counterregulation). In diabetes the glucagon response to hypoglycaemia becomes compromised and chronic hyperglucagonemia appears. There is increasing awareness that glucagon excess may underlie important manifestations of diabetes. However opinions differ widely how glucose controls glucagon secretion. The autonomous nervous system plays an important role in the glucagon response to hypoglycaemia. But it is clear that glucose controls glucagon secretion also by mechanisms involving direct effects on alpha-cells or indirect effects via paracrine factors released from non-alpha-cells within the pancreatic islets. The present review discusses these mechanisms and argues that different regulatory processes are involved in a glucose concentration-dependent manner. Direct glucose effects on the a-cell and autocrine mechanisms are probably most significant for the glucagon response to hypoglycaemia. During hyperglycaemia, when secretion from beta-and delta-cells is stimulated, paracrine inhibitory factors generate pulsatile glucagon release in opposite phase to pulsatile release of insulin and somatostatin. High concentrations of glucose have also stimulatory effects on glucagon secretion that tend to balance and even exceed the inhibitory influence. The latter actions might underlie the paradoxical hyperglucagonemia that aggravates hyperglycaemia in persons with diabetes.

Place, publisher, year, edition, pages
2014. Vol. 103, no 1, 1-10 p.
Keyword [en]
Glucagon secretion
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:uu:diva-220739DOI: 10.1016/j.diabres.2013.11.019ISI: 000330572000001OAI: oai:DiVA.org:uu-220739DiVA: diva2:707606
Available from: 2014-03-25 Created: 2014-03-20 Last updated: 2017-12-05Bibliographically approved

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Gylfe, Erik

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