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KMID : 1200020150390010001
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Diabetes & Metabolism Journal
2015 Volume.39 No. 1 p.1 ~ p.9
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Pancreatic α-Cell Dysfunction in Type 2 Diabetes: Old Kids on the Block
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Moon Jun-Sung
Won Kyu-Chang
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Abstract
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Type 2 diabetes (T2D) has been known as ’bi-hormonal disorder’ since decades ago, the role of glucagon from α-cell has languished whereas β-cell taking center stage. Recently, numerous findings indicate that the defects of glucagon secretion get involve with development and exacerbation of hyperglycemia in T2D. Aberrant α-cell responses exhibit both fasting and postprandial states: hyperglucagonemia contributes to fasting hyperglycemia caused by inappropriate hepatic glucose production, and to postprandial hyperglycemia owing to blunted α-cell suppression. During hypoglycemia, insufficient counter-regulation response is also observed in advanced T2D. Though many debates still remained for exact mechanisms behind the dysregulation of α-cell in T2D, it is clear that the blockade of glucagon receptor or suppression of glucagon secretion from α-cell would be novel therapeutic targets for control of hyperglycemia. Whereas there have not been remarkable advances in developing new class of drugs, currently available glucagon-like peptide-1 and dipeptidyl peptidase-IV inhibitors could be options for treatment of hyperglucagonemia. In this review, we focus on α-cell dysfunction and therapeutic potentials of targeting α-cell in T2D.
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KEYWORD
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Diabetes mellitus, type 2, Glucagon, Glucagon-secreting cells, Insulin, Insulin-secreting cells
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