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because of their causal association with diabetes mellitus. For this reason, α cell research has been somewhat neglected, leaving many unanswered questions about α cell biology. However, in recent years, α cell research has gained momentum due to the
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understanding of the physiology of glucagon, its potential role in the causation of diabetes, and its synergistic effects with other gut hormones in regulating metabolism. In this review article, we aim to summarize the known effects of glucagon and its
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Department of Physiology, Institute of Neuroscience and Physiology, Metabolic Research Unit, University of Gothenburg, Göteborg, Sweden
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CNC - Center for Neuroscience and Cell Biology, CIBB - Centre for Innovative Biomedicine and Biotechnology, University of Coimbra, Coimbra, Portugal
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hyperglycaemia ( Göke 2008 ). This secretory pattern becomes defective in diabetes and leads to glycaemic volatility: failure to secrete glucagon at low glucose contributes to the occurrence of hypoglycaemia ( Cryer & Gerich 1985 ), while hyperglucagonemia at
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Department of Medicine, Université de Montréal, Montréal, QC, Canada
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Department of Medicine, University of Washington, Seattle, Washington, USA
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first-line treatment for severe hypoglycemia since the 1950s ( Elrick et al. 1958 ). Dysregulation of glucagon secretion is a key feature of both major forms of diabetes, leading to the concept that diabetes is a bihormonal disorder ( Unger & Orci 1975
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-threatening hypoglycemia via the actions of glucagon on peripheral organs, thereby opposing the peripheral effects of β cell-derived insulin on glucose homeostasis. Additionally, multiple lines of evidence have implicated the α cell in disease, most notably diabetes. Early
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Division of Diabetes, Endocrinology, & Metabolism, Vanderbilt University Medical Center School of Medicine, Nashville, Tennessee, USA
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fasting response ( Felig et al. 1969 a , Marliss et al. 1970 ) but also in the development of metabolic diseases such as diabetes ( Müller et al. 1970 ). Although the hormone was discovered 100 years ago, we are still debating the regulatory
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using C-peptide-negative subjects with type 1 diabetes, who presumably had no endogenous insulin secretion, had no such augmentation of arginine-induced glucagon secretion. The authors concluded that inhibition of beta cell function and insulin secretion
