Pancreatic α-cell dysfunction in type 2 diabetes: Old kids on the block

Title
Pancreatic α-cell dysfunction in type 2 diabetes: Old kids on the block
Author(s)
원규장문준성
Keywords
antidiabetic agent; dipeptidyl peptidase IV inhibitor; glucagon; glucagon antagonist; glucagon like peptide 1; glucose; hormone antagonist; unclassified drug; bariatric surgery; cell damage; cell function; diabetogenesis; diet restriction; disease course; disease exacerbation; disease severity; glucagon release; human; hyperglucagonemia; hyperglycemia; non insulin dependent diabetes mellitus; nonhuman; pancreas islet alpha cell; pancreas islet beta cell; postprandial state; regulatory mechanism; Review
Issue Date
201502
Citation
Diabetes and Metabolism Journal, v.39, no.1, pp.1 - 9
Abstract
Type 2 diabetes (T2D) has been known as 'bi-hormonal disorder' since decades ago, the role of glucagon from ��-cell has languished whereas ��-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 ��-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 ��-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 ��-cell in T2D, it is clear that the blockade of glucagon receptor or suppression of glucagon secretion from ��-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 ��-cell dysfunction and therapeutic potentials of targeting ��-cell in T2D.
URI
http://hdl.handle.net/YU.REPOSITORY/33417http://dx.doi.org/10.4093/dmj.2015.39.1.1
ISSN
2233-6079
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의과대학 > 내과학교실 > Articles
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