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Pancreatic alpha-Cell Dysfunction in Type 2 Diabetes: Old Kids on the Block
Article em En | WPRIM | ID: wpr-42466
Biblioteca responsável: WPRO
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.
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Texto completo: 1 Índice: WPRIM Assunto principal: Glucagon / Jejum / Receptores de Glucagon / Diabetes Mellitus Tipo 2 / Células Secretoras de Glucagon / Células Secretoras de Insulina / Peptídeo 1 Semelhante ao Glucagon / Glucose / Hiperglicemia / Hipoglicemia Idioma: En Revista: Diabetes & Metabolism Journal Ano de publicação: 2015 Tipo de documento: Article
Texto completo: 1 Índice: WPRIM Assunto principal: Glucagon / Jejum / Receptores de Glucagon / Diabetes Mellitus Tipo 2 / Células Secretoras de Glucagon / Células Secretoras de Insulina / Peptídeo 1 Semelhante ao Glucagon / Glucose / Hiperglicemia / Hipoglicemia Idioma: En Revista: Diabetes & Metabolism Journal Ano de publicação: 2015 Tipo de documento: Article