| Originalsprog | Engelsk |
|---|---|
| Titel | Diapedia : The living textbook of diabetes |
| Antal sider | 3 |
| Forlag | European Association for the Study of Diabetes (EASD) |
| Publikationsdato | 12 jun. 2014 |
| Sider | 1-3 |
| Kapitel | Metabolism, Incretins, Incretin physiology and its history, Incretin secretion: direct mechanisms |
| DOI | |
| Status | Udgivet - 12 jun. 2014 |
Abstract
The incretin hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) are secreted from gastro-intestinal K- and L-cells, respectively, and play an important role in post-prandial blood glucose regulation. They do this by direct stimulation of the pancreatic β-cell, accounting for some 25-70% of postprandial insulin secretion in healthy subjects. In patients with type 2 diabetes (T2D, however, this effect is greatly reduced or lost due to a combination of severely impaired or eliminated insulinotrophic effect of GIP and reduced meal stimulated GLP-1 secretion. This suggests that the therapeutic potential of GIP for the treatment for T2D is limited, whereas GLP-1 based treatments have been on the market since 2005. Research is now pursuing novel approaches to utilize the effects of GLP-1 for T2D treatment. A combinatorial approach by which the activity of the major enzyme responsible for incretin degradation (dipeptidyl peptidase-4) is inhibited (drugs are already on the market) while the secretion of endogenous GLP-1 secretion is stimulated at the same time may prove particularly rewarding. In this section we review current knowledge on the mechanisms for direct activation of GIP and GLP-1 secretion.
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