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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With standardization of measurement of glycated hemoglobin (A1C), the International Expert Committee Report in 2009 and the American Diabetes Association in 2010 recommended incorporating A1C ≥6.5% into the previous diagnostic criteria using fasting plasma glucose and/or 2-hour plasma glucose. Whereas the association of A1C with cardiovascular diseases and other diabetic microvascular complications was linear without evidence of a distinct threshold, several studies suggested a threshold value for A1C in diabetic retinopathy (DR). In studies about the optimal cutoff value for A1C in DR, the A1C values range from 5.2% to 7.8%. There are several possible reasons why these values for DR differ so widely (differences in the definition and/or methods for DR, variation in statistical methods, differences in study population, differences in exclusion criteria, and difference in methods for measuring A1C). With these wide variations in the study method, drawing a conclusive cutoff value for A1C in DR is impossible. In published studies, the cutoff values for moderate or severe DR were higher than those for any or mild DR (6.4% to 7.0% vs. 5.5% to 6.5%).

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