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01.12.2014 | Review | Ausgabe 1/2014 Open Access

Diabetology & Metabolic Syndrome 1/2014

The role of glucagon on type 2 diabetes at a glance

Zeitschrift:
Diabetology & Metabolic Syndrome > Ausgabe 1/2014
Autor:
Amélio F Godoy-Matos
Wichtige Hinweise

Electronic supplementary material

The online version of this article (doi:10.​1186/​1758-5996-6-91) contains supplementary material, which is available to authorized users.

Competing interests

AG-M has received honoraria for lectures, travel support and consultancy services from pharmaceutical companies manufacturing diabetes treatments, including Novartis, Novo Nordisk and Takeda. He was also a Principal Investigator for clinical trials involving GLP-1RA from Sanofi-Aventis.

Abstract

The opposite effects of insulin and glucagon in fuel homeostasis, the paracrine/endocrine inhibitory effects of insulin on glucagon secretion and the hyperglucagonemia in the pathogenesis of type 2 diabetes (T2D) have long been recognized. Inappropriately increased alpha-cell function importantly contributes to hyperglycemia and reflects the loss of tonic restraint normally exerted by high local concentrations of insulin on alpha-cells, possibly as a result of beta-cell failure and alpha-cell insulin resistance, but additional mechanisms, such as the participation of incretin hormones in this response, have also been suggested. Three classes of drugs already available for clinical use address the abnormalities of glucagon secretion in T2D, namely, the GLP-1 receptor agonists (GLP-1RA), the inhibitors of dipeptidyl peptidase-4 (DPP-4i) and the amylin agonist pramlintide; it has been proposed that the glucagonostatic and insulinotropic effects of GLP-1RA equally contribute to their hypoglycemic efficacy. In this review, the control of glucagon secretion and its participation in T2D pathogenesis are summarized.
Zusatzmaterial
Authors’ original file for figure 1
13098_2014_352_MOESM1_ESM.tif
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