Pancreatic alpha-Cell Dysfunction in Type 2 Diabetes: Old Kids on the Block.
- Author:
Jun Sung MOON
1
;
Kyu Chang WON
Author Information
- Publication Type:Review
- Keywords: Diabetes mellitus, type 2; Glucagon; Glucagon-secreting cells; Insulin; Insulin-secreting cells
- MeSH: Diabetes Mellitus, Type 2; Fasting; Glucagon; Glucagon-Like Peptide 1; Glucagon-Secreting Cells; Glucose; Hyperglycemia; Hypoglycemia; Insulin; Insulin-Secreting Cells; Receptors, Glucagon
- From:Diabetes & Metabolism Journal 2015;39(1):1-9
- CountryRepublic of Korea
- Language:English
- Abstract: Type 2 diabetes (T2D) has been known as 'bi-hormonal disorder' since decades ago, the role of glucagon from alpha-cell has languished whereas beta-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 alpha-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 alpha-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 alpha-cell in T2D, it is clear that the blockade of glucagon receptor or suppression of glucagon secretion from alpha-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 alpha-cell dysfunction and therapeutic potentials of targeting alpha-cell in T2D.
